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class="documents-container backbone-social-profile-documents" style="width: 100%;"><div class="u-taCenter"></div><div class="profile--tab_content_container js-tab-pane tab-pane active" id="all"><div class="profile--tab_heading_container js-section-heading" data-section="Papers" id="Papers"><h3 class="profile--tab_heading_container">Papers by Shasta Sabo</h3></div><div class="js-work-strip profile--work_container" data-work-id="65207395"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207395/The_Amyloid_Precursor_Protein_and_Its_Regulatory_Protein_FE_65_in_Growth_Cones_and_Synapses_In_Vitro_and_In_Vivo"><img alt="Research paper thumbnail of The Amyloid Precursor Protein and Its Regulatory Protein , FE 65 , in Growth Cones and Synapses In Vitro and In Vivo" class="work-thumbnail" src="https://attachments.academia-assets.com/76907912/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207395/The_Amyloid_Precursor_Protein_and_Its_Regulatory_Protein_FE_65_in_Growth_Cones_and_Synapses_In_Vitro_and_In_Vivo">The Amyloid Precursor Protein and Its Regulatory Protein , FE 65 , in Growth Cones and Synapses In Vitro and In Vivo</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Although the Alzheimer amyloid protein precursor (APP) has been studied intensely for more than a...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Although the Alzheimer amyloid protein precursor (APP) has been studied intensely for more than a decade, its function in neurons is unresolved. Much less is known about its binding partner FE65. We have shown recently that APP and FE65 synergistically regulate the movement of transfected cells. It remained to be shown whether endogenous APP and FE65 could play a similar role in vivo. Here, we show that FE65, like APP, is expressed at high levels in neurons. Using a combination of immunofluorescence, live imaging, and subcellular fractionation, we find that FE65 and APP localize in vitro and in vivo to the most motile regions of neurons, the growth cones. Within growth cones, APP and FE65 concentrate in actin-rich lamellipodia. Finally, APP and FE65 interact in nerve terminals, where they associate with Rab5-containing synaptic organelles but not with synaptic vesicles. Our data are consistent with a role for the APP/FE65 complex in regulation of actin-based membrane motility in neu...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2457ef0e3fa7b037be56e85a5fef2ac5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":76907912,"asset_id":65207395,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/76907912/download_file?st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207395"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207395"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207395; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207395]").text(description); $(".js-view-count[data-work-id=65207395]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207395; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207395']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207395, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "2457ef0e3fa7b037be56e85a5fef2ac5" } } $('.js-work-strip[data-work-id=65207395]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207395,"title":"The Amyloid Precursor Protein and Its Regulatory Protein , FE 65 , in Growth Cones and Synapses In Vitro and In Vivo","translated_title":"","metadata":{"abstract":"Although the Alzheimer amyloid protein precursor (APP) has been studied intensely for more than a decade, its function in neurons is unresolved. 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$a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207394"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207394/Erratum_Somatostatin_diversity_in_the_inhibitory_population_Journal_of_Neuroscience_July_19_2006_7545_7546_"><img alt="Research paper thumbnail of Erratum: Somatostatin diversity in the inhibitory population (Journal of Neuroscience (July 19, 2006) (7545-7546))" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" 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class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207390/An_Autism_Associated_de_novo_Mutation_in_GluN2B_Destabilizes_Growing_Dendrites_by_Promoting_Retraction_and_Pruning">An Autism-Associated de novo Mutation in GluN2B Destabilizes Growing Dendrites by Promoting Retraction and Pruning</a></div><div class="wp-workCard_item"><span>Frontiers in Cellular Neuroscience</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Mutations in GRIN2B, which encodes the GluN2B subunit of NMDA receptors, lead to autism spectrum ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Mutations in GRIN2B, which encodes the GluN2B subunit of NMDA receptors, lead to autism spectrum disorders (ASD), but the pathophysiological mechanisms remain unclear. Recently, we showed that a GluN2B variant that is associated with severe ASD (GluN2B724t) impairs dendrite morphogenesis. To determine which aspects of dendrite growth are affected by GluN2B724t, we investigated the dynamics of dendrite growth and branching in rat neocortical neurons using time-lapse imaging. GluN2B724t expression shifted branch motility toward retraction and away from extension. GluN2B724t and wild-type neurons formed new branches at similar rates, but mutant neurons exhibited increased pruning of dendritic branches. The observed changes in dynamics resulted in nearly complete elimination of the net expansion of arbor size and complexity that is normally observed during this developmental period. These data demonstrate that ASD-associated mutant GluN2B interferes with dendrite morphogenesis by reduci...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207390"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207390"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207390; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207390]").text(description); $(".js-view-count[data-work-id=65207390]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207390; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207390']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207390, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207390]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207390,"title":"An Autism-Associated de novo Mutation in GluN2B Destabilizes Growing Dendrites by Promoting Retraction and Pruning","translated_title":"","metadata":{"abstract":"Mutations in GRIN2B, which encodes the GluN2B subunit of NMDA receptors, lead to autism spectrum disorders (ASD), but the pathophysiological mechanisms remain unclear. Recently, we showed that a GluN2B variant that is associated with severe ASD (GluN2B724t) impairs dendrite morphogenesis. To determine which aspects of dendrite growth are affected by GluN2B724t, we investigated the dynamics of dendrite growth and branching in rat neocortical neurons using time-lapse imaging. GluN2B724t expression shifted branch motility toward retraction and away from extension. GluN2B724t and wild-type neurons formed new branches at similar rates, but mutant neurons exhibited increased pruning of dendritic branches. The observed changes in dynamics resulted in nearly complete elimination of the net expansion of arbor size and complexity that is normally observed during this developmental period. These data demonstrate that ASD-associated mutant GluN2B interferes with dendrite morphogenesis by reduci...","publisher":"Frontiers Media SA","publication_name":"Frontiers in Cellular Neuroscience"},"translated_abstract":"Mutations in GRIN2B, which encodes the GluN2B subunit of NMDA receptors, lead to autism spectrum disorders (ASD), but the pathophysiological mechanisms remain unclear. Recently, we showed that a GluN2B variant that is associated with severe ASD (GluN2B724t) impairs dendrite morphogenesis. To determine which aspects of dendrite growth are affected by GluN2B724t, we investigated the dynamics of dendrite growth and branching in rat neocortical neurons using time-lapse imaging. GluN2B724t expression shifted branch motility toward retraction and away from extension. GluN2B724t and wild-type neurons formed new branches at similar rates, but mutant neurons exhibited increased pruning of dendritic branches. The observed changes in dynamics resulted in nearly complete elimination of the net expansion of arbor size and complexity that is normally observed during this developmental period. These data demonstrate that ASD-associated mutant GluN2B interferes with dendrite morphogenesis by reduci...","internal_url":"https://www.academia.edu/65207390/An_Autism_Associated_de_novo_Mutation_in_GluN2B_Destabilizes_Growing_Dendrites_by_Promoting_Retraction_and_Pruning","translated_internal_url":"","created_at":"2021-12-20T09:53:14.943-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"An_Autism_Associated_de_novo_Mutation_in_GluN2B_Destabilizes_Growing_Dendrites_by_Promoting_Retraction_and_Pruning","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[],"urls":[{"id":15439291,"url":"https://www.frontiersin.org/articles/10.3389/fncel.2021.692232/full"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207389"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207389/Effect_of_extracellular_vesicles_from_S_aureus_challenged_human_neutrophils_on_macrophages"><img alt="Research paper thumbnail of Effect of extracellular vesicles from S. aureus ‐challenged human neutrophils on macrophages" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207389/Effect_of_extracellular_vesicles_from_S_aureus_challenged_human_neutrophils_on_macrophages">Effect of extracellular vesicles from S. aureus ‐challenged human neutrophils on macrophages</a></div><div class="wp-workCard_item"><span>Journal of Leukocyte Biology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Staphylococcus aureus enhances neutrophil extracellular vesicle (EV) production. To investigate w...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Staphylococcus aureus enhances neutrophil extracellular vesicle (EV) production. To investigate whether S. aureus viability influences EV biogenesis, EVs were isolated from human neutrophils incubated with viable bacteria (bEVs) or heat‐killed bacteria (heat‐killed EVs). Protein analysis, nanoparticle tracking and transmission electron microscopy showed comparable EV production between subsets, and both viable and nonviable bacteria were also detected in respective EV subsets. As anticipated, S. aureus, as well as bEVs with viable bacteria, were proinflammatory, and killing bacteria with gentamicin reduced cytokine production to baseline levels. Although heat‐killed bacteria induced macrophage IL‐6 production, heat‐killed EVs did not. Additionally, we found that human and bacterial DNA associated with bEVs, but not heat‐killed EVs, and that the DNA association could be partially decreased by disrupting electrostatic interactions. We investigated the potential for DNA isolated from EVs (EV‐DNA) or EVs to cause inflammation. Although liposomal encapsulation of EV‐DNA increased IL‐6 production from baseline by 7.5‐fold, treatment of bEVs with DNase I had no effect on IL‐6 and IL‐1β production, suggesting that the DNA did not contribute to the inflammatory response. Filtered EVs, which lacked DNA and associated bacteria, exhibited less proinflammatory activity relative to bEVs, and enhanced macrophage expression of CD86 and HLA‐DR. Ultimately, we show that bEVs isolated by differential centrifugation co‐purify with bacteria and DNA, and studying their concerted activity and relative contribution to immune response is important to the study of host‐pathogen interactions.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207389"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207389"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207389; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207389]").text(description); $(".js-view-count[data-work-id=65207389]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207389; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207389']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207389, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207389]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207389,"title":"Effect of extracellular vesicles from S. aureus ‐challenged human neutrophils on macrophages","translated_title":"","metadata":{"abstract":"Staphylococcus aureus enhances neutrophil extracellular vesicle (EV) production. To investigate whether S. aureus viability influences EV biogenesis, EVs were isolated from human neutrophils incubated with viable bacteria (bEVs) or heat‐killed bacteria (heat‐killed EVs). Protein analysis, nanoparticle tracking and transmission electron microscopy showed comparable EV production between subsets, and both viable and nonviable bacteria were also detected in respective EV subsets. As anticipated, S. aureus, as well as bEVs with viable bacteria, were proinflammatory, and killing bacteria with gentamicin reduced cytokine production to baseline levels. Although heat‐killed bacteria induced macrophage IL‐6 production, heat‐killed EVs did not. Additionally, we found that human and bacterial DNA associated with bEVs, but not heat‐killed EVs, and that the DNA association could be partially decreased by disrupting electrostatic interactions. We investigated the potential for DNA isolated from EVs (EV‐DNA) or EVs to cause inflammation. Although liposomal encapsulation of EV‐DNA increased IL‐6 production from baseline by 7.5‐fold, treatment of bEVs with DNase I had no effect on IL‐6 and IL‐1β production, suggesting that the DNA did not contribute to the inflammatory response. Filtered EVs, which lacked DNA and associated bacteria, exhibited less proinflammatory activity relative to bEVs, and enhanced macrophage expression of CD86 and HLA‐DR. Ultimately, we show that bEVs isolated by differential centrifugation co‐purify with bacteria and DNA, and studying their concerted activity and relative contribution to immune response is important to the study of host‐pathogen interactions.","publisher":"Wiley","publication_name":"Journal of Leukocyte Biology"},"translated_abstract":"Staphylococcus aureus enhances neutrophil extracellular vesicle (EV) production. To investigate whether S. aureus viability influences EV biogenesis, EVs were isolated from human neutrophils incubated with viable bacteria (bEVs) or heat‐killed bacteria (heat‐killed EVs). Protein analysis, nanoparticle tracking and transmission electron microscopy showed comparable EV production between subsets, and both viable and nonviable bacteria were also detected in respective EV subsets. As anticipated, S. aureus, as well as bEVs with viable bacteria, were proinflammatory, and killing bacteria with gentamicin reduced cytokine production to baseline levels. Although heat‐killed bacteria induced macrophage IL‐6 production, heat‐killed EVs did not. Additionally, we found that human and bacterial DNA associated with bEVs, but not heat‐killed EVs, and that the DNA association could be partially decreased by disrupting electrostatic interactions. We investigated the potential for DNA isolated from EVs (EV‐DNA) or EVs to cause inflammation. Although liposomal encapsulation of EV‐DNA increased IL‐6 production from baseline by 7.5‐fold, treatment of bEVs with DNase I had no effect on IL‐6 and IL‐1β production, suggesting that the DNA did not contribute to the inflammatory response. Filtered EVs, which lacked DNA and associated bacteria, exhibited less proinflammatory activity relative to bEVs, and enhanced macrophage expression of CD86 and HLA‐DR. Ultimately, we show that bEVs isolated by differential centrifugation co‐purify with bacteria and DNA, and studying their concerted activity and relative contribution to immune response is important to the study of host‐pathogen interactions.","internal_url":"https://www.academia.edu/65207389/Effect_of_extracellular_vesicles_from_S_aureus_challenged_human_neutrophils_on_macrophages","translated_internal_url":"","created_at":"2021-12-20T09:53:14.769-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Effect_of_extracellular_vesicles_from_S_aureus_challenged_human_neutrophils_on_macrophages","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":1290,"name":"Immunology","url":"https://www.academia.edu/Documents/in/Immunology"}],"urls":[{"id":15439290,"url":"https://onlinelibrary.wiley.com/doi/pdf/10.1002/JLB.3AB0320-156R"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207388"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207388/Acute_neurotoxicant_exposure_induces_hyperexcitability_in_mouse_lumbar_spinal_motor_neurons"><img alt="Research paper thumbnail of Acute neurotoxicant exposure induces hyperexcitability in mouse lumbar spinal motor neurons" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207388/Acute_neurotoxicant_exposure_induces_hyperexcitability_in_mouse_lumbar_spinal_motor_neurons">Acute neurotoxicant exposure induces hyperexcitability in mouse lumbar spinal motor neurons</a></div><div class="wp-workCard_item"><span>Journal of Neurophysiology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Spinal motor neurons (MNs) are susceptible to glutamatergic excitotoxicity, an effect associated ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Spinal motor neurons (MNs) are susceptible to glutamatergic excitotoxicity, an effect associated with lumbar MN degeneration in amyotrophic lateral sclerosis (ALS). MN susceptibility to environmental toxicant exposure, one prospective contributor to sporadic ALS, has not been systematically studied. The goal of this study was to test the ability of a well-known environmental neurotoxicant to induce hyperexcitability in mouse lumbar MNs. Methylmercury (MeHg) causes neurotoxicity through mechanisms involving elevated intracellular Ca2+ concentration ([Ca2+]i), a hallmark of excitotoxicity. We tested whether acute exposure to MeHg induces hyperexcitability in MNs by altering synaptic transmission, using whole cell patch-clamp recordings of lumbar spinal MNs in vitro. Acute MeHg exposure (20 μM) led to an increase in the frequency of both spontaneous excitatory postsynaptic currents (EPSCs) and miniature EPSCs. The frequency of inhibitory postsynaptic currents (IPSCs) was also increased...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207388"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207388"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207388; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207388]").text(description); $(".js-view-count[data-work-id=65207388]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207388; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207388']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207388, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207388]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207388,"title":"Acute neurotoxicant exposure induces hyperexcitability in mouse lumbar spinal motor neurons","translated_title":"","metadata":{"abstract":"Spinal motor neurons (MNs) are susceptible to glutamatergic excitotoxicity, an effect associated with lumbar MN degeneration in amyotrophic lateral sclerosis (ALS). MN susceptibility to environmental toxicant exposure, one prospective contributor to sporadic ALS, has not been systematically studied. The goal of this study was to test the ability of a well-known environmental neurotoxicant to induce hyperexcitability in mouse lumbar MNs. Methylmercury (MeHg) causes neurotoxicity through mechanisms involving elevated intracellular Ca2+ concentration ([Ca2+]i), a hallmark of excitotoxicity. We tested whether acute exposure to MeHg induces hyperexcitability in MNs by altering synaptic transmission, using whole cell patch-clamp recordings of lumbar spinal MNs in vitro. Acute MeHg exposure (20 μM) led to an increase in the frequency of both spontaneous excitatory postsynaptic currents (EPSCs) and miniature EPSCs. The frequency of inhibitory postsynaptic currents (IPSCs) was also increased...","publisher":"American Physiological Society","publication_name":"Journal of Neurophysiology"},"translated_abstract":"Spinal motor neurons (MNs) are susceptible to glutamatergic excitotoxicity, an effect associated with lumbar MN degeneration in amyotrophic lateral sclerosis (ALS). MN susceptibility to environmental toxicant exposure, one prospective contributor to sporadic ALS, has not been systematically studied. The goal of this study was to test the ability of a well-known environmental neurotoxicant to induce hyperexcitability in mouse lumbar MNs. Methylmercury (MeHg) causes neurotoxicity through mechanisms involving elevated intracellular Ca2+ concentration ([Ca2+]i), a hallmark of excitotoxicity. We tested whether acute exposure to MeHg induces hyperexcitability in MNs by altering synaptic transmission, using whole cell patch-clamp recordings of lumbar spinal MNs in vitro. Acute MeHg exposure (20 μM) led to an increase in the frequency of both spontaneous excitatory postsynaptic currents (EPSCs) and miniature EPSCs. The frequency of inhibitory postsynaptic currents (IPSCs) was also increased...","internal_url":"https://www.academia.edu/65207388/Acute_neurotoxicant_exposure_induces_hyperexcitability_in_mouse_lumbar_spinal_motor_neurons","translated_internal_url":"","created_at":"2021-12-20T09:53:14.593-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Acute_neurotoxicant_exposure_induces_hyperexcitability_in_mouse_lumbar_spinal_motor_neurons","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":22272,"name":"Neurophysiology","url":"https://www.academia.edu/Documents/in/Neurophysiology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":2922956,"name":"Psychology and Cognitive Sciences","url":"https://www.academia.edu/Documents/in/Psychology_and_Cognitive_Sciences"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":15439289,"url":"https://journals.physiology.org/doi/pdf/10.1152/jn.00775.2019"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207387"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207387/Spatio_temporal_dynamics_of_neocortical_presynaptic_terminal_development_using_multi_photon_imaging_of_the_corpus_callosum_in_vivo"><img alt="Research paper thumbnail of Spatio-temporal dynamics of neocortical presynaptic terminal development using multi-photon imaging of the corpus callosum in vivo" class="work-thumbnail" src="https://attachments.academia-assets.com/76907914/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207387/Spatio_temporal_dynamics_of_neocortical_presynaptic_terminal_development_using_multi_photon_imaging_of_the_corpus_callosum_in_vivo">Spatio-temporal dynamics of neocortical presynaptic terminal development using multi-photon imaging of the corpus callosum in vivo</a></div><div class="wp-workCard_item"><span>Scientific Reports</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Within the developing central nervous system, the dynamics of synapse formation and elimination a...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Within the developing central nervous system, the dynamics of synapse formation and elimination are insufficiently understood. It is ideal to study these processes in vivo, where neurons form synapses within appropriate behavioral and anatomical contexts. In vivo analysis is particularly important for long-range connections, since their development cannot be adequately studied in vitro. The corpus callosum (CC) represents a clinically-relevant long-range connection since several neurodevelopmental diseases involve CC defects. Here, we present a novel strategy for in vivo longitudinal and rapid time-lapse imaging of CC presynaptic terminal development. In postnatal mice, the time-course of CC presynaptic terminal formation and elimination was highly variable between axons or groups of axons. Young presynaptic terminals were remarkably dynamic – moving, dividing to generate more boutons, and merging to consolidate small terminals into large boutons. As synaptic networks matured, presy...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b4253b7f9bdd63ca4ccf91db432048c3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":76907914,"asset_id":65207387,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/76907914/download_file?st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207387"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207387"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207387; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207387]").text(description); $(".js-view-count[data-work-id=65207387]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207387; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207387']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207387, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "b4253b7f9bdd63ca4ccf91db432048c3" } } $('.js-work-strip[data-work-id=65207387]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207387,"title":"Spatio-temporal dynamics of neocortical presynaptic terminal development using multi-photon imaging of the corpus callosum in vivo","translated_title":"","metadata":{"abstract":"Within the developing central nervous system, the dynamics of synapse formation and elimination are insufficiently understood. It is ideal to study these processes in vivo, where neurons form synapses within appropriate behavioral and anatomical contexts. In vivo analysis is particularly important for long-range connections, since their development cannot be adequately studied in vitro. The corpus callosum (CC) represents a clinically-relevant long-range connection since several neurodevelopmental diseases involve CC defects. Here, we present a novel strategy for in vivo longitudinal and rapid time-lapse imaging of CC presynaptic terminal development. In postnatal mice, the time-course of CC presynaptic terminal formation and elimination was highly variable between axons or groups of axons. Young presynaptic terminals were remarkably dynamic – moving, dividing to generate more boutons, and merging to consolidate small terminals into large boutons. As synaptic networks matured, presy...","publisher":"Springer Science and Business Media LLC","publication_name":"Scientific Reports"},"translated_abstract":"Within the developing central nervous system, the dynamics of synapse formation and elimination are insufficiently understood. It is ideal to study these processes in vivo, where neurons form synapses within appropriate behavioral and anatomical contexts. In vivo analysis is particularly important for long-range connections, since their development cannot be adequately studied in vitro. The corpus callosum (CC) represents a clinically-relevant long-range connection since several neurodevelopmental diseases involve CC defects. Here, we present a novel strategy for in vivo longitudinal and rapid time-lapse imaging of CC presynaptic terminal development. In postnatal mice, the time-course of CC presynaptic terminal formation and elimination was highly variable between axons or groups of axons. Young presynaptic terminals were remarkably dynamic – moving, dividing to generate more boutons, and merging to consolidate small terminals into large boutons. As synaptic networks matured, presy...","internal_url":"https://www.academia.edu/65207387/Spatio_temporal_dynamics_of_neocortical_presynaptic_terminal_development_using_multi_photon_imaging_of_the_corpus_callosum_in_vivo","translated_internal_url":"","created_at":"2021-12-20T09:53:14.423-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":76907914,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/76907914/thumbnails/1.jpg","file_name":"s41598-019-50431-6.pdf","download_url":"https://www.academia.edu/attachments/76907914/download_file?st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Spatio_temporal_dynamics_of_neocortical.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/76907914/s41598-019-50431-6-libre.pdf?1640025480=\u0026response-content-disposition=attachment%3B+filename%3DSpatio_temporal_dynamics_of_neocortical.pdf\u0026Expires=1732437806\u0026Signature=CUMcNofZdF8mFqsI0wbgoNQbPxCbwjkd3xWsf0-F6O6rapDypHs67vmQo~n4AE~J2d8B2toJm2FR0eY5QvybuqJMXza24Xy5dT0N8jVSHj-VQgOP~oKtpNdzEDnS1v-kpartZBFRsYUFaipiQUF~sZ1B7ecTeY257KjQwZUuT~cB3Idyy6V9iFbq4yGXGOGH~bFB2QeN31xCfpGDOoK1JVOTjKyUCAUMPa6DvheGOOJc0NiP4rMhhyZ80Ee1necCHSxhPwyrf9o7v~Irl1OmJMdxLsmMdQ41PrvxOq7NVaX~U67uQGE4XWV~QJXpc5N-VVlQfUPu7FRIfhjdwdHo7Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Spatio_temporal_dynamics_of_neocortical_presynaptic_terminal_development_using_multi_photon_imaging_of_the_corpus_callosum_in_vivo","translated_slug":"","page_count":12,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[{"id":76907914,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/76907914/thumbnails/1.jpg","file_name":"s41598-019-50431-6.pdf","download_url":"https://www.academia.edu/attachments/76907914/download_file?st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Spatio_temporal_dynamics_of_neocortical.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/76907914/s41598-019-50431-6-libre.pdf?1640025480=\u0026response-content-disposition=attachment%3B+filename%3DSpatio_temporal_dynamics_of_neocortical.pdf\u0026Expires=1732437806\u0026Signature=CUMcNofZdF8mFqsI0wbgoNQbPxCbwjkd3xWsf0-F6O6rapDypHs67vmQo~n4AE~J2d8B2toJm2FR0eY5QvybuqJMXza24Xy5dT0N8jVSHj-VQgOP~oKtpNdzEDnS1v-kpartZBFRsYUFaipiQUF~sZ1B7ecTeY257KjQwZUuT~cB3Idyy6V9iFbq4yGXGOGH~bFB2QeN31xCfpGDOoK1JVOTjKyUCAUMPa6DvheGOOJc0NiP4rMhhyZ80Ee1necCHSxhPwyrf9o7v~Irl1OmJMdxLsmMdQ41PrvxOq7NVaX~U67uQGE4XWV~QJXpc5N-VVlQfUPu7FRIfhjdwdHo7Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"},{"id":76907915,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/76907915/thumbnails/1.jpg","file_name":"s41598-019-50431-6.pdf","download_url":"https://www.academia.edu/attachments/76907915/download_file","bulk_download_file_name":"Spatio_temporal_dynamics_of_neocortical.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/76907915/s41598-019-50431-6-libre.pdf?1640025480=\u0026response-content-disposition=attachment%3B+filename%3DSpatio_temporal_dynamics_of_neocortical.pdf\u0026Expires=1732437806\u0026Signature=UJqjPFw7WYcVJFsCbfVsGL04oMZO3sjhfVMF3Kgz9ngVzsSjf6dfDdoFbqLjz9-4KUxNVtadNhqyhQM6dE7QQSjSl9BKLNSkraGrClTIfO~7FTaFAeNHB5ZLqvZoDuL4ybdVfWiJdBRctg4tt599y8KMY~-i5Foi71l0uUqgMrGQ~ArGLfjBz5NwgjHHN5pk~CjcmQ-8~IFnjjJygl2dv5V0DVSyXXwTCKtSciJGF2WaqX94q-TE1t75GFi27JahrzArXYnTPfaPCJxpshAbUltjBxerKXTUJ9572OkOf14lZSpZiJ0ta3-qJ7TJE8v-lV~bSm2139NdMJD6JenQUA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"}],"urls":[{"id":15439288,"url":"http://www.nature.com/articles/s41598-019-50431-6.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207386"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207386/A_GluN2B_mutation_identified_in_Autism_prevents_NMDA_receptor_trafficking_and_interferes_with_dendrite_growth"><img alt="Research paper thumbnail of A GluN2B mutation identified in Autism prevents NMDA receptor trafficking and interferes with dendrite growth" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207386/A_GluN2B_mutation_identified_in_Autism_prevents_NMDA_receptor_trafficking_and_interferes_with_dendrite_growth">A GluN2B mutation identified in Autism prevents NMDA receptor trafficking and interferes with dendrite growth</a></div><div class="wp-workCard_item"><span>Journal of Cell Science</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Autism spectrum disorders (ASD) are neurodevelopmental disorders with multiple genetic associatio...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Autism spectrum disorders (ASD) are neurodevelopmental disorders with multiple genetic associations. Analysis of de novo mutations identified GRIN2B, which encodes the GluN2B subunit of NMDA receptors, as a high-probability ASD gene. However, the mechanisms by which GRIN2B mutations contribute to ASD pathophysiology are not understood. Here, we investigated the cellular phenotypes induced by a human mutation that is predicted to truncate GluN2B within the extracellular loop. This mutation abolished NMDA-dependent calcium influx. Mutant GluN2B co-assembled with GluN1 but was not trafficked to the cell surface or dendrites. When mutant GluN2B was expressed in developing cortical neurons, dendrites appeared underdeveloped, with shorter and fewer branches, while spine density was unaffected. Mutant dendritic arbors were often dysmorphic, displaying abnormal filopodial-like structures. Interestingly, dendrite maldevelopment appeared when mutant GluN2B was expressed on a wild-type backgro...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207386"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207386"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207386; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207386]").text(description); $(".js-view-count[data-work-id=65207386]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207386; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207386']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207386, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207386]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207386,"title":"A GluN2B mutation identified in Autism prevents NMDA receptor trafficking and interferes with dendrite growth","translated_title":"","metadata":{"abstract":"Autism spectrum disorders (ASD) are neurodevelopmental disorders with multiple genetic associations. Analysis of de novo mutations identified GRIN2B, which encodes the GluN2B subunit of NMDA receptors, as a high-probability ASD gene. However, the mechanisms by which GRIN2B mutations contribute to ASD pathophysiology are not understood. Here, we investigated the cellular phenotypes induced by a human mutation that is predicted to truncate GluN2B within the extracellular loop. This mutation abolished NMDA-dependent calcium influx. Mutant GluN2B co-assembled with GluN1 but was not trafficked to the cell surface or dendrites. When mutant GluN2B was expressed in developing cortical neurons, dendrites appeared underdeveloped, with shorter and fewer branches, while spine density was unaffected. Mutant dendritic arbors were often dysmorphic, displaying abnormal filopodial-like structures. Interestingly, dendrite maldevelopment appeared when mutant GluN2B was expressed on a wild-type backgro...","publisher":"The Company of Biologists","publication_name":"Journal of Cell Science"},"translated_abstract":"Autism spectrum disorders (ASD) are neurodevelopmental disorders with multiple genetic associations. Analysis of de novo mutations identified GRIN2B, which encodes the GluN2B subunit of NMDA receptors, as a high-probability ASD gene. However, the mechanisms by which GRIN2B mutations contribute to ASD pathophysiology are not understood. Here, we investigated the cellular phenotypes induced by a human mutation that is predicted to truncate GluN2B within the extracellular loop. This mutation abolished NMDA-dependent calcium influx. Mutant GluN2B co-assembled with GluN1 but was not trafficked to the cell surface or dendrites. When mutant GluN2B was expressed in developing cortical neurons, dendrites appeared underdeveloped, with shorter and fewer branches, while spine density was unaffected. Mutant dendritic arbors were often dysmorphic, displaying abnormal filopodial-like structures. Interestingly, dendrite maldevelopment appeared when mutant GluN2B was expressed on a wild-type backgro...","internal_url":"https://www.academia.edu/65207386/A_GluN2B_mutation_identified_in_Autism_prevents_NMDA_receptor_trafficking_and_interferes_with_dendrite_growth","translated_internal_url":"","created_at":"2021-12-20T09:53:14.255-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"A_GluN2B_mutation_identified_in_Autism_prevents_NMDA_receptor_trafficking_and_interferes_with_dendrite_growth","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":15439287,"url":"https://syndication.highwire.org/content/doi/10.1242/jcs.232892"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207385"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207385/Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS"><img alt="Research paper thumbnail of Building a Terminal: Mechanisms of Presynaptic Development in the CNS" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207385/Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS">Building a Terminal: Mechanisms of Presynaptic Development in the CNS</a></div><div class="wp-workCard_item"><span>The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry</span><span>, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">To create a presynaptic terminal, molecular signaling events must be orchestrated across a number...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">To create a presynaptic terminal, molecular signaling events must be orchestrated across a number of subcellular compartments. In the soma, presynaptic proteins need to be synthesized, packaged together, and attached to microtubule motors for shipment through the axon. Within the axon, transport of presynaptic packages is regulated to ensure that developing synapses receive an adequate supply of components. At individual axonal sites, extracellular interactions must be translated into intracellular signals that can incorporate mobile transport vesicles into the nascent presynaptic terminal. Even once the initial recruitment process is complete, the components and subsequent functionality of presynaptic terminals need to constantly be remodeled. Perhaps most remarkably, all of these processes need to be coordinated in space and time. In this review, we discuss how these dynamic cellular processes occur in neurons of the central nervous system in order to generate presynaptic terminal...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207385"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207385"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207385; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207385]").text(description); $(".js-view-count[data-work-id=65207385]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207385; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207385']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207385, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207385]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207385,"title":"Building a Terminal: Mechanisms of Presynaptic Development in the CNS","translated_title":"","metadata":{"abstract":"To create a presynaptic terminal, molecular signaling events must be orchestrated across a number of subcellular compartments. In the soma, presynaptic proteins need to be synthesized, packaged together, and attached to microtubule motors for shipment through the axon. Within the axon, transport of presynaptic packages is regulated to ensure that developing synapses receive an adequate supply of components. At individual axonal sites, extracellular interactions must be translated into intracellular signals that can incorporate mobile transport vesicles into the nascent presynaptic terminal. Even once the initial recruitment process is complete, the components and subsequent functionality of presynaptic terminals need to constantly be remodeled. Perhaps most remarkably, all of these processes need to be coordinated in space and time. In this review, we discuss how these dynamic cellular processes occur in neurons of the central nervous system in order to generate presynaptic terminal...","publication_date":{"day":null,"month":null,"year":2016,"errors":{}},"publication_name":"The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry"},"translated_abstract":"To create a presynaptic terminal, molecular signaling events must be orchestrated across a number of subcellular compartments. In the soma, presynaptic proteins need to be synthesized, packaged together, and attached to microtubule motors for shipment through the axon. Within the axon, transport of presynaptic packages is regulated to ensure that developing synapses receive an adequate supply of components. At individual axonal sites, extracellular interactions must be translated into intracellular signals that can incorporate mobile transport vesicles into the nascent presynaptic terminal. Even once the initial recruitment process is complete, the components and subsequent functionality of presynaptic terminals need to constantly be remodeled. Perhaps most remarkably, all of these processes need to be coordinated in space and time. In this review, we discuss how these dynamic cellular processes occur in neurons of the central nervous system in order to generate presynaptic terminal...","internal_url":"https://www.academia.edu/65207385/Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS","translated_internal_url":"","created_at":"2021-12-20T09:53:14.143-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":61474,"name":"Brain","url":"https://www.academia.edu/Documents/in/Brain"},{"id":62285,"name":"Neuropeptides","url":"https://www.academia.edu/Documents/in/Neuropeptides"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":193974,"name":"Neurons","url":"https://www.academia.edu/Documents/in/Neurons"},{"id":1457054,"name":"Protein Transport","url":"https://www.academia.edu/Documents/in/Protein_Transport"},{"id":2922956,"name":"Psychology and Cognitive Sciences","url":"https://www.academia.edu/Documents/in/Psychology_and_Cognitive_Sciences"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207384"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207384/Treatment_and_prevention_of_neurodegenerative_diseases_using_modulators_of_Fe65"><img alt="Research paper thumbnail of Treatment and prevention of neurodegenerative diseases using modulators of Fe65" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207384/Treatment_and_prevention_of_neurodegenerative_diseases_using_modulators_of_Fe65">Treatment and prevention of neurodegenerative diseases using modulators of Fe65</a></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207384"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207384"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207384; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207384]").text(description); $(".js-view-count[data-work-id=65207384]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207384; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207384']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207384, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207383"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207383/App_Localization_and_Trafficking_in_the_Central_Nervous_System"><img alt="Research paper thumbnail of App Localization and Trafficking in the Central Nervous System" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207383/App_Localization_and_Trafficking_in_the_Central_Nervous_System">App Localization and Trafficking in the Central Nervous System</a></div><div class="wp-workCard_item"><span>Advances in Behavioral Biology</span><span>, 1998</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">One of the hallmarks of Alzheimer’s disease (AD) pathology is amyloid plaque deposition in the br...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">One of the hallmarks of Alzheimer’s disease (AD) pathology is amyloid plaque deposition in the brain (reviewed in Sisodia and Price, 1995). The amyloid plaque core consists primarily of a 4 kDa peptide known as β-amyloid or Aβ. Aβ is derived by proteolytic processing of a type I integral membrane protein, the amyloid Aβ protein precursor, or APP. Based on strong genetic and biochemical data (reviewed in Hardy and Duff, 1993), it is widely agreed that at least some forms of AD are caused by excess Aβ deposition in the brain, particularly excess Aβ of 42 or 43 amino acids in length (Aβ 1-42/43). The genetic evidence includes the identification of five distinct mutations in APP, all of which cosegregate with rare forms of AD: four of these mutations have been shown to increase the levels of Aβ 1-42/43. More recently, AD-associated mutations in the presenilin-1 and presenilin-2 genes have also been shown to cause increased levels of Aβl-42/43 (e.g., Scheuner et al., 1996). Finally, it has been suggested that the AD-associated form of apolipoprotein E is involved in the accumulation of Aβ (e.g., Strittmatter et al., 1993; Strittmatter et al., 1993).</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207383"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207383"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207383; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207383]").text(description); $(".js-view-count[data-work-id=65207383]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207383; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207383']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207383, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207383]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207383,"title":"App Localization and Trafficking in the Central Nervous System","translated_title":"","metadata":{"abstract":"One of the hallmarks of Alzheimer’s disease (AD) pathology is amyloid plaque deposition in the brain (reviewed in Sisodia and Price, 1995). The amyloid plaque core consists primarily of a 4 kDa peptide known as β-amyloid or Aβ. Aβ is derived by proteolytic processing of a type I integral membrane protein, the amyloid Aβ protein precursor, or APP. Based on strong genetic and biochemical data (reviewed in Hardy and Duff, 1993), it is widely agreed that at least some forms of AD are caused by excess Aβ deposition in the brain, particularly excess Aβ of 42 or 43 amino acids in length (Aβ 1-42/43). The genetic evidence includes the identification of five distinct mutations in APP, all of which cosegregate with rare forms of AD: four of these mutations have been shown to increase the levels of Aβ 1-42/43. More recently, AD-associated mutations in the presenilin-1 and presenilin-2 genes have also been shown to cause increased levels of Aβl-42/43 (e.g., Scheuner et al., 1996). Finally, it has been suggested that the AD-associated form of apolipoprotein E is involved in the accumulation of Aβ (e.g., Strittmatter et al., 1993; Strittmatter et al., 1993).","publisher":"Springer US","publication_date":{"day":null,"month":null,"year":1998,"errors":{}},"publication_name":"Advances in Behavioral Biology"},"translated_abstract":"One of the hallmarks of Alzheimer’s disease (AD) pathology is amyloid plaque deposition in the brain (reviewed in Sisodia and Price, 1995). The amyloid plaque core consists primarily of a 4 kDa peptide known as β-amyloid or Aβ. Aβ is derived by proteolytic processing of a type I integral membrane protein, the amyloid Aβ protein precursor, or APP. Based on strong genetic and biochemical data (reviewed in Hardy and Duff, 1993), it is widely agreed that at least some forms of AD are caused by excess Aβ deposition in the brain, particularly excess Aβ of 42 or 43 amino acids in length (Aβ 1-42/43). The genetic evidence includes the identification of five distinct mutations in APP, all of which cosegregate with rare forms of AD: four of these mutations have been shown to increase the levels of Aβ 1-42/43. More recently, AD-associated mutations in the presenilin-1 and presenilin-2 genes have also been shown to cause increased levels of Aβl-42/43 (e.g., Scheuner et al., 1996). Finally, it has been suggested that the AD-associated form of apolipoprotein E is involved in the accumulation of Aβ (e.g., Strittmatter et al., 1993; Strittmatter et al., 1993).","internal_url":"https://www.academia.edu/65207383/App_Localization_and_Trafficking_in_the_Central_Nervous_System","translated_internal_url":"","created_at":"2021-12-20T09:53:13.799-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"App_Localization_and_Trafficking_in_the_Central_Nervous_System","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":620289,"name":"Behavioral Biology","url":"https://www.academia.edu/Documents/in/Behavioral_Biology"}],"urls":[{"id":15439285,"url":"http://link.springer.com/content/pdf/10.1007/978-1-4615-5337-3_70.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207382"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207382/Regulation_of_APP_Metabolism_by_Protein_Phosphorylation"><img alt="Research paper thumbnail of Regulation of APP Metabolism by Protein Phosphorylation" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207382/Regulation_of_APP_Metabolism_by_Protein_Phosphorylation">Regulation of APP Metabolism by Protein Phosphorylation</a></div><div class="wp-workCard_item"><span>Advances in Behavioral Biology</span><span>, 1998</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A hallmark of Alzheimer disease (AD) is the build-up of an amyloid protein (Aβ) (Glenner and Wong...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">A hallmark of Alzheimer disease (AD) is the build-up of an amyloid protein (Aβ) (Glenner and Wong, 1984, Masters et al., 1985) in the brain parenchyma and in the cere-brovasculature (Tomlinson and Corsellis, 1984). Aβ is derived from a large transmembrane precursor, the amyloid protein precursor (APP) (Goldgaber et al., 1987, Kang et al., 1987, Kitaguchi et al., 1988, Ponte et al., 1988, Robakis et al., 1987, Tanzi et al., 1987, Tanzi et al., 1988). For a variety of reasons, many researchers believe that the build-up of Aβ in the brain causes the synaptic loss and associated dementia which occurs in AD. These reasons include the observation that one of the several mutations (hereafter referred to as the Swedish mutation, Mullan et al., 1992) in APP which cosegregate with AD is associated with abnormally high production of Aβ (Cai et al., 1993, Citron et al., 1992). It therefore seems plausible to argue that increased production of Aβ might underlie the symptoms of AD in individuals bearing this mutation. More recently it has been shown that an allele of apolipoprotein E (ApoE(4)) is associated with forms of AD (Corder et al., 1993, Strittmatter et al., 1993). This allele of ApoE is especially prone to inducing the aggregation and precipitation of Aβ in vitro. In the case of individuals with ApoE(4) it is possible that there is an associated increase in Aβ deposition (Schmechel et al., 1993) which again might underlie the symptoms of AD. Thus, there is evidence to suggest that both increased Aβ production and decreased Aβ clearance may contribute to AD. From these findings it is a small jump to argue that decreasing Aβ formation and/or increasing Aβ clearance might slow the progression of AD.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207382"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207382"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207382; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207382]").text(description); $(".js-view-count[data-work-id=65207382]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207382; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207382']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207382, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207382]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207382,"title":"Regulation of APP Metabolism by Protein Phosphorylation","translated_title":"","metadata":{"abstract":"A hallmark of Alzheimer disease (AD) is the build-up of an amyloid protein (Aβ) (Glenner and Wong, 1984, Masters et al., 1985) in the brain parenchyma and in the cere-brovasculature (Tomlinson and Corsellis, 1984). Aβ is derived from a large transmembrane precursor, the amyloid protein precursor (APP) (Goldgaber et al., 1987, Kang et al., 1987, Kitaguchi et al., 1988, Ponte et al., 1988, Robakis et al., 1987, Tanzi et al., 1987, Tanzi et al., 1988). For a variety of reasons, many researchers believe that the build-up of Aβ in the brain causes the synaptic loss and associated dementia which occurs in AD. These reasons include the observation that one of the several mutations (hereafter referred to as the Swedish mutation, Mullan et al., 1992) in APP which cosegregate with AD is associated with abnormally high production of Aβ (Cai et al., 1993, Citron et al., 1992). It therefore seems plausible to argue that increased production of Aβ might underlie the symptoms of AD in individuals bearing this mutation. More recently it has been shown that an allele of apolipoprotein E (ApoE(4)) is associated with forms of AD (Corder et al., 1993, Strittmatter et al., 1993). This allele of ApoE is especially prone to inducing the aggregation and precipitation of Aβ in vitro. In the case of individuals with ApoE(4) it is possible that there is an associated increase in Aβ deposition (Schmechel et al., 1993) which again might underlie the symptoms of AD. Thus, there is evidence to suggest that both increased Aβ production and decreased Aβ clearance may contribute to AD. From these findings it is a small jump to argue that decreasing Aβ formation and/or increasing Aβ clearance might slow the progression of AD.","publication_date":{"day":null,"month":null,"year":1998,"errors":{}},"publication_name":"Advances in Behavioral Biology"},"translated_abstract":"A hallmark of Alzheimer disease (AD) is the build-up of an amyloid protein (Aβ) (Glenner and Wong, 1984, Masters et al., 1985) in the brain parenchyma and in the cere-brovasculature (Tomlinson and Corsellis, 1984). Aβ is derived from a large transmembrane precursor, the amyloid protein precursor (APP) (Goldgaber et al., 1987, Kang et al., 1987, Kitaguchi et al., 1988, Ponte et al., 1988, Robakis et al., 1987, Tanzi et al., 1987, Tanzi et al., 1988). For a variety of reasons, many researchers believe that the build-up of Aβ in the brain causes the synaptic loss and associated dementia which occurs in AD. These reasons include the observation that one of the several mutations (hereafter referred to as the Swedish mutation, Mullan et al., 1992) in APP which cosegregate with AD is associated with abnormally high production of Aβ (Cai et al., 1993, Citron et al., 1992). It therefore seems plausible to argue that increased production of Aβ might underlie the symptoms of AD in individuals bearing this mutation. More recently it has been shown that an allele of apolipoprotein E (ApoE(4)) is associated with forms of AD (Corder et al., 1993, Strittmatter et al., 1993). This allele of ApoE is especially prone to inducing the aggregation and precipitation of Aβ in vitro. In the case of individuals with ApoE(4) it is possible that there is an associated increase in Aβ deposition (Schmechel et al., 1993) which again might underlie the symptoms of AD. Thus, there is evidence to suggest that both increased Aβ production and decreased Aβ clearance may contribute to AD. From these findings it is a small jump to argue that decreasing Aβ formation and/or increasing Aβ clearance might slow the progression of AD.","internal_url":"https://www.academia.edu/65207382/Regulation_of_APP_Metabolism_by_Protein_Phosphorylation","translated_internal_url":"","created_at":"2021-12-20T09:53:13.660-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Regulation_of_APP_Metabolism_by_Protein_Phosphorylation","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":620289,"name":"Behavioral Biology","url":"https://www.academia.edu/Documents/in/Behavioral_Biology"}],"urls":[]}, dispatcherData: dispatcherData }); 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It is well established that experience modifies circuit development. Therefore, understanding how synapse formation is controlled by synaptic activity is a key question in neuroscience. In this review, we focus on the regulation of excitatory presynaptic terminal development by glutamate, the predominant excitatory neurotransmitter in the brain. We discuss the evidence that NMDA receptor activation mediates these effects of glutamate and present the hypothesis that local activation of presynaptic NMDA receptors (preNMDARs) contributes to glutamate-dependent control of presynaptic development. Abnormal glutamate signaling and aberrant synapse development are both thought to contribute to the pathogenesis of a variety of neurodevelopmental disorders, including autism spectrum disorders, intellectual disability, epilepsy, anxiety, depression, and schizophrenia. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207380"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207380/Targeting_amyloid_beta_Cytosolic_protein_protein_interactions_that_regulate_the_amyloid_precursor_protein"><img alt="Research paper thumbnail of Targeting amyloid beta : Cytosolic protein-protein interactions that regulate the amyloid precursor protein" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207380/Targeting_amyloid_beta_Cytosolic_protein_protein_interactions_that_regulate_the_amyloid_precursor_protein">Targeting amyloid beta : Cytosolic protein-protein interactions that regulate the amyloid precursor protein</a></div><div class="wp-workCard_item"><span>Drug Development Research</span><span>, 2002</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207380"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207380"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207380; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207379"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207379/Regulation_of_amyloid_protein_precursor_processing_trafficking_and_function_by_FE65_and_APP_binding_protein_"><img alt="Research paper thumbnail of Regulation of amyloid protein precursor processing, trafficking and function by FE65, and APP-binding protein /" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207379/Regulation_of_amyloid_protein_precursor_processing_trafficking_and_function_by_FE65_and_APP_binding_protein_">Regulation of amyloid protein precursor processing, trafficking and function by FE65, and APP-binding protein /</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A thesis presented to the faculty of The Rockefeller University in partial fulfillment of the req...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">A thesis presented to the faculty of The Rockefeller University in partial fulfillment of the requirements for the degree of Doctor of Philosophy. Thesis (Ph. D.)--Rockefeller University, 2000. Includes bibliographical references (p. 243-265).</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207379"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207379"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207379; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207379]").text(description); $(".js-view-count[data-work-id=65207379]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207379; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207379']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207379, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207379]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207379,"title":"Regulation of amyloid protein precursor processing, trafficking and function by FE65, and APP-binding protein /","translated_title":"","metadata":{"abstract":"A thesis presented to the faculty of The Rockefeller University in partial fulfillment of the requirements for the degree of Doctor of Philosophy. Thesis (Ph. D.)--Rockefeller University, 2000. Includes bibliographical references (p. 243-265)."},"translated_abstract":"A thesis presented to the faculty of The Rockefeller University in partial fulfillment of the requirements for the degree of Doctor of Philosophy. Thesis (Ph. D.)--Rockefeller University, 2000. Includes bibliographical references (p. 243-265).","internal_url":"https://www.academia.edu/65207379/Regulation_of_amyloid_protein_precursor_processing_trafficking_and_function_by_FE65_and_APP_binding_protein_","translated_internal_url":"","created_at":"2021-12-20T09:53:13.167-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Regulation_of_amyloid_protein_precursor_processing_trafficking_and_function_by_FE65_and_APP_binding_protein_","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207378"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207378/Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS"><img alt="Research paper thumbnail of Building a Terminal: Mechanisms of Presynaptic Development in the CNS" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207378/Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS">Building a Terminal: Mechanisms of Presynaptic Development in the CNS</a></div><div class="wp-workCard_item"><span>The Neuroscientist</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">To create a presynaptic terminal, molecular signaling events must be orchestrated across a number...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">To create a presynaptic terminal, molecular signaling events must be orchestrated across a number of subcellular compartments. In the soma, presynaptic proteins need to be synthesized, packaged together, and attached to microtubule motors for shipment through the axon. Within the axon, transport of presynaptic packages is regulated to ensure that developing synapses receive an adequate supply of components. At individual axonal sites, extracellular interactions must be translated into intracellular signals that can incorporate mobile transport vesicles into the nascent presynaptic terminal. Even once the initial recruitment process is complete, the components and subsequent functionality of presynaptic terminals need to constantly be remodeled. Perhaps most remarkably, all of these processes need to be coordinated in space and time. In this review, we discuss how these dynamic cellular processes occur in neurons of the central nervous system in order to generate presynaptic terminal...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207378"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207378"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207378; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207378]").text(description); $(".js-view-count[data-work-id=65207378]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207378; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207378']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207378, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207378]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207378,"title":"Building a Terminal: Mechanisms of Presynaptic Development in the CNS","translated_title":"","metadata":{"abstract":"To create a presynaptic terminal, molecular signaling events must be orchestrated across a number of subcellular compartments. 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Perhaps most remarkably, all of these processes need to be coordinated in space and time. In this review, we discuss how these dynamic cellular processes occur in neurons of the central nervous system in order to generate presynaptic terminal...","internal_url":"https://www.academia.edu/65207378/Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS","translated_internal_url":"","created_at":"2021-12-20T09:53:13.042-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":61474,"name":"Brain","url":"https://www.academia.edu/Documents/in/Brain"},{"id":62285,"name":"Neuropeptides","url":"https://www.academia.edu/Documents/in/Neuropeptides"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":193974,"name":"Neurons","url":"https://www.academia.edu/Documents/in/Neurons"},{"id":1457054,"name":"Protein Transport","url":"https://www.academia.edu/Documents/in/Protein_Transport"},{"id":2922956,"name":"Psychology and Cognitive Sciences","url":"https://www.academia.edu/Documents/in/Psychology_and_Cognitive_Sciences"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[]}, dispatcherData: dispatcherData }); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207376"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207376/Dynamic_mechanisms_of_neuroligin_dependent_presynaptic_terminal_assembly_in_living_cortical_neurons"><img alt="Research paper thumbnail of Dynamic mechanisms of neuroligin-dependent presynaptic terminal assembly in living cortical neurons" class="work-thumbnail" src="https://attachments.academia-assets.com/76908007/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207376/Dynamic_mechanisms_of_neuroligin_dependent_presynaptic_terminal_assembly_in_living_cortical_neurons">Dynamic mechanisms of neuroligin-dependent presynaptic terminal assembly in living cortical neurons</a></div><div class="wp-workCard_item"><span>Neural development</span><span>, Jan 29, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Synapse formation occurs when synaptogenic signals trigger coordinated development of pre and pos...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Synapse formation occurs when synaptogenic signals trigger coordinated development of pre and postsynaptic structures. One of the best-characterized synaptogenic signals is trans-synaptic adhesion. However, it remains unclear how synaptic proteins are recruited to sites of adhesion. In particular, it is unknown whether synaptogenic signals attract synaptic vesicle (SV) and active zone (AZ) proteins to nascent synapses or instead predominantly function to create sites that are capable of forming synapses. It is also unclear how labile synaptic proteins are at developing synapses after their initial recruitment. To address these issues, we used long-term, live confocal imaging of presynaptic terminal formation in cultured cortical neurons after contact with the synaptogenic postsynaptic adhesion proteins neuroligin-1 or SynCAM-1. Surprisingly, we find that trans-synaptic adhesion does not attract SV or AZ proteins nor alter their transport. In addition, although neurexin (the presynap...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bc23bd66cfcd199b6961f55a586cc156" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":76908007,"asset_id":65207376,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/76908007/download_file?st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207376"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207376"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207376; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207376]").text(description); $(".js-view-count[data-work-id=65207376]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207376; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207376']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207376, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "bc23bd66cfcd199b6961f55a586cc156" } } $('.js-work-strip[data-work-id=65207376]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207376,"title":"Dynamic mechanisms of neuroligin-dependent presynaptic terminal assembly in living cortical neurons","translated_title":"","metadata":{"abstract":"Synapse formation occurs when synaptogenic signals trigger coordinated development of pre and postsynaptic structures. One of the best-characterized synaptogenic signals is trans-synaptic adhesion. However, it remains unclear how synaptic proteins are recruited to sites of adhesion. In particular, it is unknown whether synaptogenic signals attract synaptic vesicle (SV) and active zone (AZ) proteins to nascent synapses or instead predominantly function to create sites that are capable of forming synapses. It is also unclear how labile synaptic proteins are at developing synapses after their initial recruitment. To address these issues, we used long-term, live confocal imaging of presynaptic terminal formation in cultured cortical neurons after contact with the synaptogenic postsynaptic adhesion proteins neuroligin-1 or SynCAM-1. Surprisingly, we find that trans-synaptic adhesion does not attract SV or AZ proteins nor alter their transport. In addition, although neurexin (the presynap...","publication_date":{"day":29,"month":1,"year":2014,"errors":{}},"publication_name":"Neural development"},"translated_abstract":"Synapse formation occurs when synaptogenic signals trigger coordinated development of pre and postsynaptic structures. One of the best-characterized synaptogenic signals is trans-synaptic adhesion. However, it remains unclear how synaptic proteins are recruited to sites of adhesion. In particular, it is unknown whether synaptogenic signals attract synaptic vesicle (SV) and active zone (AZ) proteins to nascent synapses or instead predominantly function to create sites that are capable of forming synapses. It is also unclear how labile synaptic proteins are at developing synapses after their initial recruitment. To address these issues, we used long-term, live confocal imaging of presynaptic terminal formation in cultured cortical neurons after contact with the synaptogenic postsynaptic adhesion proteins neuroligin-1 or SynCAM-1. Surprisingly, we find that trans-synaptic adhesion does not attract SV or AZ proteins nor alter their transport. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> </div><div class="profile--tab_content_container js-tab-pane tab-pane" data-section-id="13333449" id="papers"><div class="js-work-strip profile--work_container" data-work-id="65207395"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207395/The_Amyloid_Precursor_Protein_and_Its_Regulatory_Protein_FE_65_in_Growth_Cones_and_Synapses_In_Vitro_and_In_Vivo"><img alt="Research paper thumbnail of The Amyloid Precursor Protein and Its Regulatory Protein , FE 65 , in Growth Cones and Synapses In Vitro and In Vivo" class="work-thumbnail" src="https://attachments.academia-assets.com/76907912/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207395/The_Amyloid_Precursor_Protein_and_Its_Regulatory_Protein_FE_65_in_Growth_Cones_and_Synapses_In_Vitro_and_In_Vivo">The Amyloid Precursor Protein and Its Regulatory Protein , FE 65 , in Growth Cones and Synapses In Vitro and In Vivo</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Although the Alzheimer amyloid protein precursor (APP) has been studied intensely for more than a...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Although the Alzheimer amyloid protein precursor (APP) has been studied intensely for more than a decade, its function in neurons is unresolved. Much less is known about its binding partner FE65. We have shown recently that APP and FE65 synergistically regulate the movement of transfected cells. It remained to be shown whether endogenous APP and FE65 could play a similar role in vivo. Here, we show that FE65, like APP, is expressed at high levels in neurons. Using a combination of immunofluorescence, live imaging, and subcellular fractionation, we find that FE65 and APP localize in vitro and in vivo to the most motile regions of neurons, the growth cones. Within growth cones, APP and FE65 concentrate in actin-rich lamellipodia. Finally, APP and FE65 interact in nerve terminals, where they associate with Rab5-containing synaptic organelles but not with synaptic vesicles. Our data are consistent with a role for the APP/FE65 complex in regulation of actin-based membrane motility in neu...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2457ef0e3fa7b037be56e85a5fef2ac5" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":76907912,"asset_id":65207395,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/76907912/download_file?st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207395"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207395"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207395; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207395]").text(description); $(".js-view-count[data-work-id=65207395]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207395; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207395']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207395, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "2457ef0e3fa7b037be56e85a5fef2ac5" } } $('.js-work-strip[data-work-id=65207395]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207395,"title":"The Amyloid Precursor Protein and Its Regulatory Protein , FE 65 , in Growth Cones and Synapses In Vitro and In Vivo","translated_title":"","metadata":{"abstract":"Although the Alzheimer amyloid protein precursor (APP) has been studied intensely for more than a decade, its function in neurons is unresolved. 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Our data are consistent with a role for the APP/FE65 complex in regulation of actin-based membrane motility in neu...","publication_date":{"day":null,"month":null,"year":2003,"errors":{}}},"translated_abstract":"Although the Alzheimer amyloid protein precursor (APP) has been studied intensely for more than a decade, its function in neurons is unresolved. Much less is known about its binding partner FE65. We have shown recently that APP and FE65 synergistically regulate the movement of transfected cells. It remained to be shown whether endogenous APP and FE65 could play a similar role in vivo. Here, we show that FE65, like APP, is expressed at high levels in neurons. Using a combination of immunofluorescence, live imaging, and subcellular fractionation, we find that FE65 and APP localize in vitro and in vivo to the most motile regions of neurons, the growth cones. Within growth cones, APP and FE65 concentrate in actin-rich lamellipodia. 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class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207390/An_Autism_Associated_de_novo_Mutation_in_GluN2B_Destabilizes_Growing_Dendrites_by_Promoting_Retraction_and_Pruning">An Autism-Associated de novo Mutation in GluN2B Destabilizes Growing Dendrites by Promoting Retraction and Pruning</a></div><div class="wp-workCard_item"><span>Frontiers in Cellular Neuroscience</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Mutations in GRIN2B, which encodes the GluN2B subunit of NMDA receptors, lead to autism spectrum ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Mutations in GRIN2B, which encodes the GluN2B subunit of NMDA receptors, lead to autism spectrum disorders (ASD), but the pathophysiological mechanisms remain unclear. Recently, we showed that a GluN2B variant that is associated with severe ASD (GluN2B724t) impairs dendrite morphogenesis. To determine which aspects of dendrite growth are affected by GluN2B724t, we investigated the dynamics of dendrite growth and branching in rat neocortical neurons using time-lapse imaging. GluN2B724t expression shifted branch motility toward retraction and away from extension. GluN2B724t and wild-type neurons formed new branches at similar rates, but mutant neurons exhibited increased pruning of dendritic branches. The observed changes in dynamics resulted in nearly complete elimination of the net expansion of arbor size and complexity that is normally observed during this developmental period. These data demonstrate that ASD-associated mutant GluN2B interferes with dendrite morphogenesis by reduci...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207390"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207390"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207390; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207390]").text(description); $(".js-view-count[data-work-id=65207390]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207390; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207390']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207390, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207390]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207390,"title":"An Autism-Associated de novo Mutation in GluN2B Destabilizes Growing Dendrites by Promoting Retraction and Pruning","translated_title":"","metadata":{"abstract":"Mutations in GRIN2B, which encodes the GluN2B subunit of NMDA receptors, lead to autism spectrum disorders (ASD), but the pathophysiological mechanisms remain unclear. Recently, we showed that a GluN2B variant that is associated with severe ASD (GluN2B724t) impairs dendrite morphogenesis. To determine which aspects of dendrite growth are affected by GluN2B724t, we investigated the dynamics of dendrite growth and branching in rat neocortical neurons using time-lapse imaging. GluN2B724t expression shifted branch motility toward retraction and away from extension. GluN2B724t and wild-type neurons formed new branches at similar rates, but mutant neurons exhibited increased pruning of dendritic branches. The observed changes in dynamics resulted in nearly complete elimination of the net expansion of arbor size and complexity that is normally observed during this developmental period. These data demonstrate that ASD-associated mutant GluN2B interferes with dendrite morphogenesis by reduci...","publisher":"Frontiers Media SA","publication_name":"Frontiers in Cellular Neuroscience"},"translated_abstract":"Mutations in GRIN2B, which encodes the GluN2B subunit of NMDA receptors, lead to autism spectrum disorders (ASD), but the pathophysiological mechanisms remain unclear. Recently, we showed that a GluN2B variant that is associated with severe ASD (GluN2B724t) impairs dendrite morphogenesis. To determine which aspects of dendrite growth are affected by GluN2B724t, we investigated the dynamics of dendrite growth and branching in rat neocortical neurons using time-lapse imaging. GluN2B724t expression shifted branch motility toward retraction and away from extension. GluN2B724t and wild-type neurons formed new branches at similar rates, but mutant neurons exhibited increased pruning of dendritic branches. The observed changes in dynamics resulted in nearly complete elimination of the net expansion of arbor size and complexity that is normally observed during this developmental period. These data demonstrate that ASD-associated mutant GluN2B interferes with dendrite morphogenesis by reduci...","internal_url":"https://www.academia.edu/65207390/An_Autism_Associated_de_novo_Mutation_in_GluN2B_Destabilizes_Growing_Dendrites_by_Promoting_Retraction_and_Pruning","translated_internal_url":"","created_at":"2021-12-20T09:53:14.943-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"An_Autism_Associated_de_novo_Mutation_in_GluN2B_Destabilizes_Growing_Dendrites_by_Promoting_Retraction_and_Pruning","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[],"urls":[{"id":15439291,"url":"https://www.frontiersin.org/articles/10.3389/fncel.2021.692232/full"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207389"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207389/Effect_of_extracellular_vesicles_from_S_aureus_challenged_human_neutrophils_on_macrophages"><img alt="Research paper thumbnail of Effect of extracellular vesicles from S. aureus ‐challenged human neutrophils on macrophages" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207389/Effect_of_extracellular_vesicles_from_S_aureus_challenged_human_neutrophils_on_macrophages">Effect of extracellular vesicles from S. aureus ‐challenged human neutrophils on macrophages</a></div><div class="wp-workCard_item"><span>Journal of Leukocyte Biology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Staphylococcus aureus enhances neutrophil extracellular vesicle (EV) production. To investigate w...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Staphylococcus aureus enhances neutrophil extracellular vesicle (EV) production. To investigate whether S. aureus viability influences EV biogenesis, EVs were isolated from human neutrophils incubated with viable bacteria (bEVs) or heat‐killed bacteria (heat‐killed EVs). Protein analysis, nanoparticle tracking and transmission electron microscopy showed comparable EV production between subsets, and both viable and nonviable bacteria were also detected in respective EV subsets. As anticipated, S. aureus, as well as bEVs with viable bacteria, were proinflammatory, and killing bacteria with gentamicin reduced cytokine production to baseline levels. Although heat‐killed bacteria induced macrophage IL‐6 production, heat‐killed EVs did not. Additionally, we found that human and bacterial DNA associated with bEVs, but not heat‐killed EVs, and that the DNA association could be partially decreased by disrupting electrostatic interactions. We investigated the potential for DNA isolated from EVs (EV‐DNA) or EVs to cause inflammation. Although liposomal encapsulation of EV‐DNA increased IL‐6 production from baseline by 7.5‐fold, treatment of bEVs with DNase I had no effect on IL‐6 and IL‐1β production, suggesting that the DNA did not contribute to the inflammatory response. Filtered EVs, which lacked DNA and associated bacteria, exhibited less proinflammatory activity relative to bEVs, and enhanced macrophage expression of CD86 and HLA‐DR. Ultimately, we show that bEVs isolated by differential centrifugation co‐purify with bacteria and DNA, and studying their concerted activity and relative contribution to immune response is important to the study of host‐pathogen interactions.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207389"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207389"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207389; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207389]").text(description); $(".js-view-count[data-work-id=65207389]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207389; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207389']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207389, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207389]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207389,"title":"Effect of extracellular vesicles from S. aureus ‐challenged human neutrophils on macrophages","translated_title":"","metadata":{"abstract":"Staphylococcus aureus enhances neutrophil extracellular vesicle (EV) production. To investigate whether S. aureus viability influences EV biogenesis, EVs were isolated from human neutrophils incubated with viable bacteria (bEVs) or heat‐killed bacteria (heat‐killed EVs). Protein analysis, nanoparticle tracking and transmission electron microscopy showed comparable EV production between subsets, and both viable and nonviable bacteria were also detected in respective EV subsets. As anticipated, S. aureus, as well as bEVs with viable bacteria, were proinflammatory, and killing bacteria with gentamicin reduced cytokine production to baseline levels. Although heat‐killed bacteria induced macrophage IL‐6 production, heat‐killed EVs did not. Additionally, we found that human and bacterial DNA associated with bEVs, but not heat‐killed EVs, and that the DNA association could be partially decreased by disrupting electrostatic interactions. We investigated the potential for DNA isolated from EVs (EV‐DNA) or EVs to cause inflammation. Although liposomal encapsulation of EV‐DNA increased IL‐6 production from baseline by 7.5‐fold, treatment of bEVs with DNase I had no effect on IL‐6 and IL‐1β production, suggesting that the DNA did not contribute to the inflammatory response. Filtered EVs, which lacked DNA and associated bacteria, exhibited less proinflammatory activity relative to bEVs, and enhanced macrophage expression of CD86 and HLA‐DR. Ultimately, we show that bEVs isolated by differential centrifugation co‐purify with bacteria and DNA, and studying their concerted activity and relative contribution to immune response is important to the study of host‐pathogen interactions.","publisher":"Wiley","publication_name":"Journal of Leukocyte Biology"},"translated_abstract":"Staphylococcus aureus enhances neutrophil extracellular vesicle (EV) production. To investigate whether S. aureus viability influences EV biogenesis, EVs were isolated from human neutrophils incubated with viable bacteria (bEVs) or heat‐killed bacteria (heat‐killed EVs). Protein analysis, nanoparticle tracking and transmission electron microscopy showed comparable EV production between subsets, and both viable and nonviable bacteria were also detected in respective EV subsets. As anticipated, S. aureus, as well as bEVs with viable bacteria, were proinflammatory, and killing bacteria with gentamicin reduced cytokine production to baseline levels. Although heat‐killed bacteria induced macrophage IL‐6 production, heat‐killed EVs did not. Additionally, we found that human and bacterial DNA associated with bEVs, but not heat‐killed EVs, and that the DNA association could be partially decreased by disrupting electrostatic interactions. We investigated the potential for DNA isolated from EVs (EV‐DNA) or EVs to cause inflammation. Although liposomal encapsulation of EV‐DNA increased IL‐6 production from baseline by 7.5‐fold, treatment of bEVs with DNase I had no effect on IL‐6 and IL‐1β production, suggesting that the DNA did not contribute to the inflammatory response. Filtered EVs, which lacked DNA and associated bacteria, exhibited less proinflammatory activity relative to bEVs, and enhanced macrophage expression of CD86 and HLA‐DR. Ultimately, we show that bEVs isolated by differential centrifugation co‐purify with bacteria and DNA, and studying their concerted activity and relative contribution to immune response is important to the study of host‐pathogen interactions.","internal_url":"https://www.academia.edu/65207389/Effect_of_extracellular_vesicles_from_S_aureus_challenged_human_neutrophils_on_macrophages","translated_internal_url":"","created_at":"2021-12-20T09:53:14.769-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Effect_of_extracellular_vesicles_from_S_aureus_challenged_human_neutrophils_on_macrophages","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":1290,"name":"Immunology","url":"https://www.academia.edu/Documents/in/Immunology"}],"urls":[{"id":15439290,"url":"https://onlinelibrary.wiley.com/doi/pdf/10.1002/JLB.3AB0320-156R"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207388"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207388/Acute_neurotoxicant_exposure_induces_hyperexcitability_in_mouse_lumbar_spinal_motor_neurons"><img alt="Research paper thumbnail of Acute neurotoxicant exposure induces hyperexcitability in mouse lumbar spinal motor neurons" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207388/Acute_neurotoxicant_exposure_induces_hyperexcitability_in_mouse_lumbar_spinal_motor_neurons">Acute neurotoxicant exposure induces hyperexcitability in mouse lumbar spinal motor neurons</a></div><div class="wp-workCard_item"><span>Journal of Neurophysiology</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Spinal motor neurons (MNs) are susceptible to glutamatergic excitotoxicity, an effect associated ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Spinal motor neurons (MNs) are susceptible to glutamatergic excitotoxicity, an effect associated with lumbar MN degeneration in amyotrophic lateral sclerosis (ALS). MN susceptibility to environmental toxicant exposure, one prospective contributor to sporadic ALS, has not been systematically studied. The goal of this study was to test the ability of a well-known environmental neurotoxicant to induce hyperexcitability in mouse lumbar MNs. Methylmercury (MeHg) causes neurotoxicity through mechanisms involving elevated intracellular Ca2+ concentration ([Ca2+]i), a hallmark of excitotoxicity. We tested whether acute exposure to MeHg induces hyperexcitability in MNs by altering synaptic transmission, using whole cell patch-clamp recordings of lumbar spinal MNs in vitro. Acute MeHg exposure (20 μM) led to an increase in the frequency of both spontaneous excitatory postsynaptic currents (EPSCs) and miniature EPSCs. The frequency of inhibitory postsynaptic currents (IPSCs) was also increased...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207388"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207388"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207388; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207388]").text(description); $(".js-view-count[data-work-id=65207388]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207388; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207388']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207388, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207388]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207388,"title":"Acute neurotoxicant exposure induces hyperexcitability in mouse lumbar spinal motor neurons","translated_title":"","metadata":{"abstract":"Spinal motor neurons (MNs) are susceptible to glutamatergic excitotoxicity, an effect associated with lumbar MN degeneration in amyotrophic lateral sclerosis (ALS). MN susceptibility to environmental toxicant exposure, one prospective contributor to sporadic ALS, has not been systematically studied. The goal of this study was to test the ability of a well-known environmental neurotoxicant to induce hyperexcitability in mouse lumbar MNs. Methylmercury (MeHg) causes neurotoxicity through mechanisms involving elevated intracellular Ca2+ concentration ([Ca2+]i), a hallmark of excitotoxicity. We tested whether acute exposure to MeHg induces hyperexcitability in MNs by altering synaptic transmission, using whole cell patch-clamp recordings of lumbar spinal MNs in vitro. Acute MeHg exposure (20 μM) led to an increase in the frequency of both spontaneous excitatory postsynaptic currents (EPSCs) and miniature EPSCs. The frequency of inhibitory postsynaptic currents (IPSCs) was also increased...","publisher":"American Physiological Society","publication_name":"Journal of Neurophysiology"},"translated_abstract":"Spinal motor neurons (MNs) are susceptible to glutamatergic excitotoxicity, an effect associated with lumbar MN degeneration in amyotrophic lateral sclerosis (ALS). MN susceptibility to environmental toxicant exposure, one prospective contributor to sporadic ALS, has not been systematically studied. The goal of this study was to test the ability of a well-known environmental neurotoxicant to induce hyperexcitability in mouse lumbar MNs. Methylmercury (MeHg) causes neurotoxicity through mechanisms involving elevated intracellular Ca2+ concentration ([Ca2+]i), a hallmark of excitotoxicity. We tested whether acute exposure to MeHg induces hyperexcitability in MNs by altering synaptic transmission, using whole cell patch-clamp recordings of lumbar spinal MNs in vitro. Acute MeHg exposure (20 μM) led to an increase in the frequency of both spontaneous excitatory postsynaptic currents (EPSCs) and miniature EPSCs. The frequency of inhibitory postsynaptic currents (IPSCs) was also increased...","internal_url":"https://www.academia.edu/65207388/Acute_neurotoxicant_exposure_induces_hyperexcitability_in_mouse_lumbar_spinal_motor_neurons","translated_internal_url":"","created_at":"2021-12-20T09:53:14.593-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Acute_neurotoxicant_exposure_induces_hyperexcitability_in_mouse_lumbar_spinal_motor_neurons","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":523,"name":"Chemistry","url":"https://www.academia.edu/Documents/in/Chemistry"},{"id":22272,"name":"Neurophysiology","url":"https://www.academia.edu/Documents/in/Neurophysiology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":2922956,"name":"Psychology and Cognitive Sciences","url":"https://www.academia.edu/Documents/in/Psychology_and_Cognitive_Sciences"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":15439289,"url":"https://journals.physiology.org/doi/pdf/10.1152/jn.00775.2019"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207387"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207387/Spatio_temporal_dynamics_of_neocortical_presynaptic_terminal_development_using_multi_photon_imaging_of_the_corpus_callosum_in_vivo"><img alt="Research paper thumbnail of Spatio-temporal dynamics of neocortical presynaptic terminal development using multi-photon imaging of the corpus callosum in vivo" class="work-thumbnail" src="https://attachments.academia-assets.com/76907914/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207387/Spatio_temporal_dynamics_of_neocortical_presynaptic_terminal_development_using_multi_photon_imaging_of_the_corpus_callosum_in_vivo">Spatio-temporal dynamics of neocortical presynaptic terminal development using multi-photon imaging of the corpus callosum in vivo</a></div><div class="wp-workCard_item"><span>Scientific Reports</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Within the developing central nervous system, the dynamics of synapse formation and elimination a...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Within the developing central nervous system, the dynamics of synapse formation and elimination are insufficiently understood. It is ideal to study these processes in vivo, where neurons form synapses within appropriate behavioral and anatomical contexts. In vivo analysis is particularly important for long-range connections, since their development cannot be adequately studied in vitro. The corpus callosum (CC) represents a clinically-relevant long-range connection since several neurodevelopmental diseases involve CC defects. Here, we present a novel strategy for in vivo longitudinal and rapid time-lapse imaging of CC presynaptic terminal development. In postnatal mice, the time-course of CC presynaptic terminal formation and elimination was highly variable between axons or groups of axons. Young presynaptic terminals were remarkably dynamic – moving, dividing to generate more boutons, and merging to consolidate small terminals into large boutons. As synaptic networks matured, presy...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="b4253b7f9bdd63ca4ccf91db432048c3" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":76907914,"asset_id":65207387,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/76907914/download_file?st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207387"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207387"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207387; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207387]").text(description); $(".js-view-count[data-work-id=65207387]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207387; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207387']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207387, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "b4253b7f9bdd63ca4ccf91db432048c3" } } $('.js-work-strip[data-work-id=65207387]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207387,"title":"Spatio-temporal dynamics of neocortical presynaptic terminal development using multi-photon imaging of the corpus callosum in vivo","translated_title":"","metadata":{"abstract":"Within the developing central nervous system, the dynamics of synapse formation and elimination are insufficiently understood. It is ideal to study these processes in vivo, where neurons form synapses within appropriate behavioral and anatomical contexts. In vivo analysis is particularly important for long-range connections, since their development cannot be adequately studied in vitro. The corpus callosum (CC) represents a clinically-relevant long-range connection since several neurodevelopmental diseases involve CC defects. Here, we present a novel strategy for in vivo longitudinal and rapid time-lapse imaging of CC presynaptic terminal development. In postnatal mice, the time-course of CC presynaptic terminal formation and elimination was highly variable between axons or groups of axons. Young presynaptic terminals were remarkably dynamic – moving, dividing to generate more boutons, and merging to consolidate small terminals into large boutons. As synaptic networks matured, presy...","publisher":"Springer Science and Business Media LLC","publication_name":"Scientific Reports"},"translated_abstract":"Within the developing central nervous system, the dynamics of synapse formation and elimination are insufficiently understood. It is ideal to study these processes in vivo, where neurons form synapses within appropriate behavioral and anatomical contexts. In vivo analysis is particularly important for long-range connections, since their development cannot be adequately studied in vitro. The corpus callosum (CC) represents a clinically-relevant long-range connection since several neurodevelopmental diseases involve CC defects. Here, we present a novel strategy for in vivo longitudinal and rapid time-lapse imaging of CC presynaptic terminal development. In postnatal mice, the time-course of CC presynaptic terminal formation and elimination was highly variable between axons or groups of axons. Young presynaptic terminals were remarkably dynamic – moving, dividing to generate more boutons, and merging to consolidate small terminals into large boutons. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207386"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207386/A_GluN2B_mutation_identified_in_Autism_prevents_NMDA_receptor_trafficking_and_interferes_with_dendrite_growth"><img alt="Research paper thumbnail of A GluN2B mutation identified in Autism prevents NMDA receptor trafficking and interferes with dendrite growth" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207386/A_GluN2B_mutation_identified_in_Autism_prevents_NMDA_receptor_trafficking_and_interferes_with_dendrite_growth">A GluN2B mutation identified in Autism prevents NMDA receptor trafficking and interferes with dendrite growth</a></div><div class="wp-workCard_item"><span>Journal of Cell Science</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Autism spectrum disorders (ASD) are neurodevelopmental disorders with multiple genetic associatio...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Autism spectrum disorders (ASD) are neurodevelopmental disorders with multiple genetic associations. Analysis of de novo mutations identified GRIN2B, which encodes the GluN2B subunit of NMDA receptors, as a high-probability ASD gene. However, the mechanisms by which GRIN2B mutations contribute to ASD pathophysiology are not understood. Here, we investigated the cellular phenotypes induced by a human mutation that is predicted to truncate GluN2B within the extracellular loop. This mutation abolished NMDA-dependent calcium influx. Mutant GluN2B co-assembled with GluN1 but was not trafficked to the cell surface or dendrites. When mutant GluN2B was expressed in developing cortical neurons, dendrites appeared underdeveloped, with shorter and fewer branches, while spine density was unaffected. Mutant dendritic arbors were often dysmorphic, displaying abnormal filopodial-like structures. Interestingly, dendrite maldevelopment appeared when mutant GluN2B was expressed on a wild-type backgro...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207386"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207386"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207386; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207386]").text(description); $(".js-view-count[data-work-id=65207386]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207386; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207386']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207386, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207386]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207386,"title":"A GluN2B mutation identified in Autism prevents NMDA receptor trafficking and interferes with dendrite growth","translated_title":"","metadata":{"abstract":"Autism spectrum disorders (ASD) are neurodevelopmental disorders with multiple genetic associations. Analysis of de novo mutations identified GRIN2B, which encodes the GluN2B subunit of NMDA receptors, as a high-probability ASD gene. However, the mechanisms by which GRIN2B mutations contribute to ASD pathophysiology are not understood. Here, we investigated the cellular phenotypes induced by a human mutation that is predicted to truncate GluN2B within the extracellular loop. This mutation abolished NMDA-dependent calcium influx. Mutant GluN2B co-assembled with GluN1 but was not trafficked to the cell surface or dendrites. When mutant GluN2B was expressed in developing cortical neurons, dendrites appeared underdeveloped, with shorter and fewer branches, while spine density was unaffected. Mutant dendritic arbors were often dysmorphic, displaying abnormal filopodial-like structures. Interestingly, dendrite maldevelopment appeared when mutant GluN2B was expressed on a wild-type backgro...","publisher":"The Company of Biologists","publication_name":"Journal of Cell Science"},"translated_abstract":"Autism spectrum disorders (ASD) are neurodevelopmental disorders with multiple genetic associations. Analysis of de novo mutations identified GRIN2B, which encodes the GluN2B subunit of NMDA receptors, as a high-probability ASD gene. However, the mechanisms by which GRIN2B mutations contribute to ASD pathophysiology are not understood. Here, we investigated the cellular phenotypes induced by a human mutation that is predicted to truncate GluN2B within the extracellular loop. This mutation abolished NMDA-dependent calcium influx. Mutant GluN2B co-assembled with GluN1 but was not trafficked to the cell surface or dendrites. When mutant GluN2B was expressed in developing cortical neurons, dendrites appeared underdeveloped, with shorter and fewer branches, while spine density was unaffected. Mutant dendritic arbors were often dysmorphic, displaying abnormal filopodial-like structures. Interestingly, dendrite maldevelopment appeared when mutant GluN2B was expressed on a wild-type backgro...","internal_url":"https://www.academia.edu/65207386/A_GluN2B_mutation_identified_in_Autism_prevents_NMDA_receptor_trafficking_and_interferes_with_dendrite_growth","translated_internal_url":"","created_at":"2021-12-20T09:53:14.255-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"A_GluN2B_mutation_identified_in_Autism_prevents_NMDA_receptor_trafficking_and_interferes_with_dendrite_growth","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[{"id":15439287,"url":"https://syndication.highwire.org/content/doi/10.1242/jcs.232892"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207385"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207385/Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS"><img alt="Research paper thumbnail of Building a Terminal: Mechanisms of Presynaptic Development in the CNS" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207385/Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS">Building a Terminal: Mechanisms of Presynaptic Development in the CNS</a></div><div class="wp-workCard_item"><span>The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry</span><span>, 2016</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">To create a presynaptic terminal, molecular signaling events must be orchestrated across a number...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">To create a presynaptic terminal, molecular signaling events must be orchestrated across a number of subcellular compartments. In the soma, presynaptic proteins need to be synthesized, packaged together, and attached to microtubule motors for shipment through the axon. Within the axon, transport of presynaptic packages is regulated to ensure that developing synapses receive an adequate supply of components. At individual axonal sites, extracellular interactions must be translated into intracellular signals that can incorporate mobile transport vesicles into the nascent presynaptic terminal. Even once the initial recruitment process is complete, the components and subsequent functionality of presynaptic terminals need to constantly be remodeled. Perhaps most remarkably, all of these processes need to be coordinated in space and time. In this review, we discuss how these dynamic cellular processes occur in neurons of the central nervous system in order to generate presynaptic terminal...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207385"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207385"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207385; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207385]").text(description); $(".js-view-count[data-work-id=65207385]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207385; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207385']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207385, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207385]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207385,"title":"Building a Terminal: Mechanisms of Presynaptic Development in the CNS","translated_title":"","metadata":{"abstract":"To create a presynaptic terminal, molecular signaling events must be orchestrated across a number of subcellular compartments. In the soma, presynaptic proteins need to be synthesized, packaged together, and attached to microtubule motors for shipment through the axon. Within the axon, transport of presynaptic packages is regulated to ensure that developing synapses receive an adequate supply of components. At individual axonal sites, extracellular interactions must be translated into intracellular signals that can incorporate mobile transport vesicles into the nascent presynaptic terminal. Even once the initial recruitment process is complete, the components and subsequent functionality of presynaptic terminals need to constantly be remodeled. Perhaps most remarkably, all of these processes need to be coordinated in space and time. In this review, we discuss how these dynamic cellular processes occur in neurons of the central nervous system in order to generate presynaptic terminal...","publication_date":{"day":null,"month":null,"year":2016,"errors":{}},"publication_name":"The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry"},"translated_abstract":"To create a presynaptic terminal, molecular signaling events must be orchestrated across a number of subcellular compartments. In the soma, presynaptic proteins need to be synthesized, packaged together, and attached to microtubule motors for shipment through the axon. Within the axon, transport of presynaptic packages is regulated to ensure that developing synapses receive an adequate supply of components. At individual axonal sites, extracellular interactions must be translated into intracellular signals that can incorporate mobile transport vesicles into the nascent presynaptic terminal. Even once the initial recruitment process is complete, the components and subsequent functionality of presynaptic terminals need to constantly be remodeled. Perhaps most remarkably, all of these processes need to be coordinated in space and time. In this review, we discuss how these dynamic cellular processes occur in neurons of the central nervous system in order to generate presynaptic terminal...","internal_url":"https://www.academia.edu/65207385/Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS","translated_internal_url":"","created_at":"2021-12-20T09:53:14.143-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":61474,"name":"Brain","url":"https://www.academia.edu/Documents/in/Brain"},{"id":62285,"name":"Neuropeptides","url":"https://www.academia.edu/Documents/in/Neuropeptides"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":193974,"name":"Neurons","url":"https://www.academia.edu/Documents/in/Neurons"},{"id":1457054,"name":"Protein Transport","url":"https://www.academia.edu/Documents/in/Protein_Transport"},{"id":2922956,"name":"Psychology and Cognitive Sciences","url":"https://www.academia.edu/Documents/in/Psychology_and_Cognitive_Sciences"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207384"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207384/Treatment_and_prevention_of_neurodegenerative_diseases_using_modulators_of_Fe65"><img alt="Research paper thumbnail of Treatment and prevention of neurodegenerative diseases using modulators of Fe65" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207384/Treatment_and_prevention_of_neurodegenerative_diseases_using_modulators_of_Fe65">Treatment and prevention of neurodegenerative diseases using modulators of Fe65</a></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207384"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207384"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207384; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207384]").text(description); $(".js-view-count[data-work-id=65207384]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207384; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207384']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207384, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207383"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207383/App_Localization_and_Trafficking_in_the_Central_Nervous_System"><img alt="Research paper thumbnail of App Localization and Trafficking in the Central Nervous System" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207383/App_Localization_and_Trafficking_in_the_Central_Nervous_System">App Localization and Trafficking in the Central Nervous System</a></div><div class="wp-workCard_item"><span>Advances in Behavioral Biology</span><span>, 1998</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">One of the hallmarks of Alzheimer’s disease (AD) pathology is amyloid plaque deposition in the br...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">One of the hallmarks of Alzheimer’s disease (AD) pathology is amyloid plaque deposition in the brain (reviewed in Sisodia and Price, 1995). The amyloid plaque core consists primarily of a 4 kDa peptide known as β-amyloid or Aβ. Aβ is derived by proteolytic processing of a type I integral membrane protein, the amyloid Aβ protein precursor, or APP. Based on strong genetic and biochemical data (reviewed in Hardy and Duff, 1993), it is widely agreed that at least some forms of AD are caused by excess Aβ deposition in the brain, particularly excess Aβ of 42 or 43 amino acids in length (Aβ 1-42/43). The genetic evidence includes the identification of five distinct mutations in APP, all of which cosegregate with rare forms of AD: four of these mutations have been shown to increase the levels of Aβ 1-42/43. More recently, AD-associated mutations in the presenilin-1 and presenilin-2 genes have also been shown to cause increased levels of Aβl-42/43 (e.g., Scheuner et al., 1996). Finally, it has been suggested that the AD-associated form of apolipoprotein E is involved in the accumulation of Aβ (e.g., Strittmatter et al., 1993; Strittmatter et al., 1993).</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207383"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207383"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207383; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207383]").text(description); $(".js-view-count[data-work-id=65207383]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207383; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207383']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207383, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207383]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207383,"title":"App Localization and Trafficking in the Central Nervous System","translated_title":"","metadata":{"abstract":"One of the hallmarks of Alzheimer’s disease (AD) pathology is amyloid plaque deposition in the brain (reviewed in Sisodia and Price, 1995). The amyloid plaque core consists primarily of a 4 kDa peptide known as β-amyloid or Aβ. Aβ is derived by proteolytic processing of a type I integral membrane protein, the amyloid Aβ protein precursor, or APP. Based on strong genetic and biochemical data (reviewed in Hardy and Duff, 1993), it is widely agreed that at least some forms of AD are caused by excess Aβ deposition in the brain, particularly excess Aβ of 42 or 43 amino acids in length (Aβ 1-42/43). The genetic evidence includes the identification of five distinct mutations in APP, all of which cosegregate with rare forms of AD: four of these mutations have been shown to increase the levels of Aβ 1-42/43. More recently, AD-associated mutations in the presenilin-1 and presenilin-2 genes have also been shown to cause increased levels of Aβl-42/43 (e.g., Scheuner et al., 1996). Finally, it has been suggested that the AD-associated form of apolipoprotein E is involved in the accumulation of Aβ (e.g., Strittmatter et al., 1993; Strittmatter et al., 1993).","publisher":"Springer US","publication_date":{"day":null,"month":null,"year":1998,"errors":{}},"publication_name":"Advances in Behavioral Biology"},"translated_abstract":"One of the hallmarks of Alzheimer’s disease (AD) pathology is amyloid plaque deposition in the brain (reviewed in Sisodia and Price, 1995). The amyloid plaque core consists primarily of a 4 kDa peptide known as β-amyloid or Aβ. Aβ is derived by proteolytic processing of a type I integral membrane protein, the amyloid Aβ protein precursor, or APP. Based on strong genetic and biochemical data (reviewed in Hardy and Duff, 1993), it is widely agreed that at least some forms of AD are caused by excess Aβ deposition in the brain, particularly excess Aβ of 42 or 43 amino acids in length (Aβ 1-42/43). The genetic evidence includes the identification of five distinct mutations in APP, all of which cosegregate with rare forms of AD: four of these mutations have been shown to increase the levels of Aβ 1-42/43. More recently, AD-associated mutations in the presenilin-1 and presenilin-2 genes have also been shown to cause increased levels of Aβl-42/43 (e.g., Scheuner et al., 1996). Finally, it has been suggested that the AD-associated form of apolipoprotein E is involved in the accumulation of Aβ (e.g., Strittmatter et al., 1993; Strittmatter et al., 1993).","internal_url":"https://www.academia.edu/65207383/App_Localization_and_Trafficking_in_the_Central_Nervous_System","translated_internal_url":"","created_at":"2021-12-20T09:53:13.799-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"App_Localization_and_Trafficking_in_the_Central_Nervous_System","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":620289,"name":"Behavioral Biology","url":"https://www.academia.edu/Documents/in/Behavioral_Biology"}],"urls":[{"id":15439285,"url":"http://link.springer.com/content/pdf/10.1007/978-1-4615-5337-3_70.pdf"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207382"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207382/Regulation_of_APP_Metabolism_by_Protein_Phosphorylation"><img alt="Research paper thumbnail of Regulation of APP Metabolism by Protein Phosphorylation" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207382/Regulation_of_APP_Metabolism_by_Protein_Phosphorylation">Regulation of APP Metabolism by Protein Phosphorylation</a></div><div class="wp-workCard_item"><span>Advances in Behavioral Biology</span><span>, 1998</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A hallmark of Alzheimer disease (AD) is the build-up of an amyloid protein (Aβ) (Glenner and Wong...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">A hallmark of Alzheimer disease (AD) is the build-up of an amyloid protein (Aβ) (Glenner and Wong, 1984, Masters et al., 1985) in the brain parenchyma and in the cere-brovasculature (Tomlinson and Corsellis, 1984). Aβ is derived from a large transmembrane precursor, the amyloid protein precursor (APP) (Goldgaber et al., 1987, Kang et al., 1987, Kitaguchi et al., 1988, Ponte et al., 1988, Robakis et al., 1987, Tanzi et al., 1987, Tanzi et al., 1988). For a variety of reasons, many researchers believe that the build-up of Aβ in the brain causes the synaptic loss and associated dementia which occurs in AD. These reasons include the observation that one of the several mutations (hereafter referred to as the Swedish mutation, Mullan et al., 1992) in APP which cosegregate with AD is associated with abnormally high production of Aβ (Cai et al., 1993, Citron et al., 1992). It therefore seems plausible to argue that increased production of Aβ might underlie the symptoms of AD in individuals bearing this mutation. More recently it has been shown that an allele of apolipoprotein E (ApoE(4)) is associated with forms of AD (Corder et al., 1993, Strittmatter et al., 1993). This allele of ApoE is especially prone to inducing the aggregation and precipitation of Aβ in vitro. In the case of individuals with ApoE(4) it is possible that there is an associated increase in Aβ deposition (Schmechel et al., 1993) which again might underlie the symptoms of AD. Thus, there is evidence to suggest that both increased Aβ production and decreased Aβ clearance may contribute to AD. From these findings it is a small jump to argue that decreasing Aβ formation and/or increasing Aβ clearance might slow the progression of AD.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207382"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207382"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207382; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207382]").text(description); $(".js-view-count[data-work-id=65207382]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207382; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207382']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207382, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207382]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207382,"title":"Regulation of APP Metabolism by Protein Phosphorylation","translated_title":"","metadata":{"abstract":"A hallmark of Alzheimer disease (AD) is the build-up of an amyloid protein (Aβ) (Glenner and Wong, 1984, Masters et al., 1985) in the brain parenchyma and in the cere-brovasculature (Tomlinson and Corsellis, 1984). Aβ is derived from a large transmembrane precursor, the amyloid protein precursor (APP) (Goldgaber et al., 1987, Kang et al., 1987, Kitaguchi et al., 1988, Ponte et al., 1988, Robakis et al., 1987, Tanzi et al., 1987, Tanzi et al., 1988). For a variety of reasons, many researchers believe that the build-up of Aβ in the brain causes the synaptic loss and associated dementia which occurs in AD. These reasons include the observation that one of the several mutations (hereafter referred to as the Swedish mutation, Mullan et al., 1992) in APP which cosegregate with AD is associated with abnormally high production of Aβ (Cai et al., 1993, Citron et al., 1992). It therefore seems plausible to argue that increased production of Aβ might underlie the symptoms of AD in individuals bearing this mutation. More recently it has been shown that an allele of apolipoprotein E (ApoE(4)) is associated with forms of AD (Corder et al., 1993, Strittmatter et al., 1993). This allele of ApoE is especially prone to inducing the aggregation and precipitation of Aβ in vitro. In the case of individuals with ApoE(4) it is possible that there is an associated increase in Aβ deposition (Schmechel et al., 1993) which again might underlie the symptoms of AD. Thus, there is evidence to suggest that both increased Aβ production and decreased Aβ clearance may contribute to AD. From these findings it is a small jump to argue that decreasing Aβ formation and/or increasing Aβ clearance might slow the progression of AD.","publication_date":{"day":null,"month":null,"year":1998,"errors":{}},"publication_name":"Advances in Behavioral Biology"},"translated_abstract":"A hallmark of Alzheimer disease (AD) is the build-up of an amyloid protein (Aβ) (Glenner and Wong, 1984, Masters et al., 1985) in the brain parenchyma and in the cere-brovasculature (Tomlinson and Corsellis, 1984). Aβ is derived from a large transmembrane precursor, the amyloid protein precursor (APP) (Goldgaber et al., 1987, Kang et al., 1987, Kitaguchi et al., 1988, Ponte et al., 1988, Robakis et al., 1987, Tanzi et al., 1987, Tanzi et al., 1988). For a variety of reasons, many researchers believe that the build-up of Aβ in the brain causes the synaptic loss and associated dementia which occurs in AD. These reasons include the observation that one of the several mutations (hereafter referred to as the Swedish mutation, Mullan et al., 1992) in APP which cosegregate with AD is associated with abnormally high production of Aβ (Cai et al., 1993, Citron et al., 1992). It therefore seems plausible to argue that increased production of Aβ might underlie the symptoms of AD in individuals bearing this mutation. More recently it has been shown that an allele of apolipoprotein E (ApoE(4)) is associated with forms of AD (Corder et al., 1993, Strittmatter et al., 1993). This allele of ApoE is especially prone to inducing the aggregation and precipitation of Aβ in vitro. In the case of individuals with ApoE(4) it is possible that there is an associated increase in Aβ deposition (Schmechel et al., 1993) which again might underlie the symptoms of AD. Thus, there is evidence to suggest that both increased Aβ production and decreased Aβ clearance may contribute to AD. From these findings it is a small jump to argue that decreasing Aβ formation and/or increasing Aβ clearance might slow the progression of AD.","internal_url":"https://www.academia.edu/65207382/Regulation_of_APP_Metabolism_by_Protein_Phosphorylation","translated_internal_url":"","created_at":"2021-12-20T09:53:13.660-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Regulation_of_APP_Metabolism_by_Protein_Phosphorylation","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":620289,"name":"Behavioral Biology","url":"https://www.academia.edu/Documents/in/Behavioral_Biology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207381"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207381/On_the_Role_of_Glutamate_in_Presynaptic_Development_Possible_Contributions_of_Presynaptic_NMDA_Receptors"><img alt="Research paper thumbnail of On the Role of Glutamate in Presynaptic Development: Possible Contributions of Presynaptic NMDA Receptors" class="work-thumbnail" src="https://attachments.academia-assets.com/76908006/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207381/On_the_Role_of_Glutamate_in_Presynaptic_Development_Possible_Contributions_of_Presynaptic_NMDA_Receptors">On the Role of Glutamate in Presynaptic Development: Possible Contributions of Presynaptic NMDA Receptors</a></div><div class="wp-workCard_item"><span>Biomolecules</span><span>, 2015</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="6977e79f548826506ea6d2a95c350c1a" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":76908006,"asset_id":65207381,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/76908006/download_file?st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207381"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207381"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207381; 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It is well established that experience modifies circuit development. Therefore, understanding how synapse formation is controlled by synaptic activity is a key question in neuroscience. In this review, we focus on the regulation of excitatory presynaptic terminal development by glutamate, the predominant excitatory neurotransmitter in the brain. We discuss the evidence that NMDA receptor activation mediates these effects of glutamate and present the hypothesis that local activation of presynaptic NMDA receptors (preNMDARs) contributes to glutamate-dependent control of presynaptic development. Abnormal glutamate signaling and aberrant synapse development are both thought to contribute to the pathogenesis of a variety of neurodevelopmental disorders, including autism spectrum disorders, intellectual disability, epilepsy, anxiety, depression, and schizophrenia. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207380"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207380/Targeting_amyloid_beta_Cytosolic_protein_protein_interactions_that_regulate_the_amyloid_precursor_protein"><img alt="Research paper thumbnail of Targeting amyloid beta : Cytosolic protein-protein interactions that regulate the amyloid precursor protein" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207380/Targeting_amyloid_beta_Cytosolic_protein_protein_interactions_that_regulate_the_amyloid_precursor_protein">Targeting amyloid beta : Cytosolic protein-protein interactions that regulate the amyloid precursor protein</a></div><div class="wp-workCard_item"><span>Drug Development Research</span><span>, 2002</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207380"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207380"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207380; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207379"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207379/Regulation_of_amyloid_protein_precursor_processing_trafficking_and_function_by_FE65_and_APP_binding_protein_"><img alt="Research paper thumbnail of Regulation of amyloid protein precursor processing, trafficking and function by FE65, and APP-binding protein /" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207379/Regulation_of_amyloid_protein_precursor_processing_trafficking_and_function_by_FE65_and_APP_binding_protein_">Regulation of amyloid protein precursor processing, trafficking and function by FE65, and APP-binding protein /</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">A thesis presented to the faculty of The Rockefeller University in partial fulfillment of the req...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">A thesis presented to the faculty of The Rockefeller University in partial fulfillment of the requirements for the degree of Doctor of Philosophy. Thesis (Ph. D.)--Rockefeller University, 2000. Includes bibliographical references (p. 243-265).</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207379"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207379"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207379; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207379]").text(description); $(".js-view-count[data-work-id=65207379]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207379; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207379']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207379, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207379]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207379,"title":"Regulation of amyloid protein precursor processing, trafficking and function by FE65, and APP-binding protein /","translated_title":"","metadata":{"abstract":"A thesis presented to the faculty of The Rockefeller University in partial fulfillment of the requirements for the degree of Doctor of Philosophy. Thesis (Ph. D.)--Rockefeller University, 2000. Includes bibliographical references (p. 243-265)."},"translated_abstract":"A thesis presented to the faculty of The Rockefeller University in partial fulfillment of the requirements for the degree of Doctor of Philosophy. Thesis (Ph. D.)--Rockefeller University, 2000. Includes bibliographical references (p. 243-265).","internal_url":"https://www.academia.edu/65207379/Regulation_of_amyloid_protein_precursor_processing_trafficking_and_function_by_FE65_and_APP_binding_protein_","translated_internal_url":"","created_at":"2021-12-20T09:53:13.167-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Regulation_of_amyloid_protein_precursor_processing_trafficking_and_function_by_FE65_and_APP_binding_protein_","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207378"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207378/Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS"><img alt="Research paper thumbnail of Building a Terminal: Mechanisms of Presynaptic Development in the CNS" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207378/Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS">Building a Terminal: Mechanisms of Presynaptic Development in the CNS</a></div><div class="wp-workCard_item"><span>The Neuroscientist</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">To create a presynaptic terminal, molecular signaling events must be orchestrated across a number...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">To create a presynaptic terminal, molecular signaling events must be orchestrated across a number of subcellular compartments. In the soma, presynaptic proteins need to be synthesized, packaged together, and attached to microtubule motors for shipment through the axon. Within the axon, transport of presynaptic packages is regulated to ensure that developing synapses receive an adequate supply of components. At individual axonal sites, extracellular interactions must be translated into intracellular signals that can incorporate mobile transport vesicles into the nascent presynaptic terminal. Even once the initial recruitment process is complete, the components and subsequent functionality of presynaptic terminals need to constantly be remodeled. Perhaps most remarkably, all of these processes need to be coordinated in space and time. In this review, we discuss how these dynamic cellular processes occur in neurons of the central nervous system in order to generate presynaptic terminal...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207378"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207378"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207378; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207378]").text(description); $(".js-view-count[data-work-id=65207378]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207378; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207378']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207378, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=65207378]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207378,"title":"Building a Terminal: Mechanisms of Presynaptic Development in the CNS","translated_title":"","metadata":{"abstract":"To create a presynaptic terminal, molecular signaling events must be orchestrated across a number of subcellular compartments. 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Perhaps most remarkably, all of these processes need to be coordinated in space and time. In this review, we discuss how these dynamic cellular processes occur in neurons of the central nervous system in order to generate presynaptic terminal...","internal_url":"https://www.academia.edu/65207378/Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS","translated_internal_url":"","created_at":"2021-12-20T09:53:13.042-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":66442384,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Building_a_Terminal_Mechanisms_of_Presynaptic_Development_in_the_CNS","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":66442384,"first_name":"Shasta","middle_initials":null,"last_name":"Sabo","page_name":"ShastaSabo","domain_name":"independent","created_at":"2017-07-14T12:54:27.501-07:00","display_name":"Shasta Sabo","url":"https://independent.academia.edu/ShastaSabo"},"attachments":[],"research_interests":[{"id":7710,"name":"Biology","url":"https://www.academia.edu/Documents/in/Biology"},{"id":26327,"name":"Medicine","url":"https://www.academia.edu/Documents/in/Medicine"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":61474,"name":"Brain","url":"https://www.academia.edu/Documents/in/Brain"},{"id":62285,"name":"Neuropeptides","url":"https://www.academia.edu/Documents/in/Neuropeptides"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":193974,"name":"Neurons","url":"https://www.academia.edu/Documents/in/Neurons"},{"id":1457054,"name":"Protein Transport","url":"https://www.academia.edu/Documents/in/Protein_Transport"},{"id":2922956,"name":"Psychology and Cognitive Sciences","url":"https://www.academia.edu/Documents/in/Psychology_and_Cognitive_Sciences"},{"id":3763225,"name":"Medical and Health Sciences","url":"https://www.academia.edu/Documents/in/Medical_and_Health_Sciences"}],"urls":[]}, dispatcherData: dispatcherData }); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="65207376"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/65207376/Dynamic_mechanisms_of_neuroligin_dependent_presynaptic_terminal_assembly_in_living_cortical_neurons"><img alt="Research paper thumbnail of Dynamic mechanisms of neuroligin-dependent presynaptic terminal assembly in living cortical neurons" class="work-thumbnail" src="https://attachments.academia-assets.com/76908007/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/65207376/Dynamic_mechanisms_of_neuroligin_dependent_presynaptic_terminal_assembly_in_living_cortical_neurons">Dynamic mechanisms of neuroligin-dependent presynaptic terminal assembly in living cortical neurons</a></div><div class="wp-workCard_item"><span>Neural development</span><span>, Jan 29, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Synapse formation occurs when synaptogenic signals trigger coordinated development of pre and pos...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Synapse formation occurs when synaptogenic signals trigger coordinated development of pre and postsynaptic structures. One of the best-characterized synaptogenic signals is trans-synaptic adhesion. However, it remains unclear how synaptic proteins are recruited to sites of adhesion. In particular, it is unknown whether synaptogenic signals attract synaptic vesicle (SV) and active zone (AZ) proteins to nascent synapses or instead predominantly function to create sites that are capable of forming synapses. It is also unclear how labile synaptic proteins are at developing synapses after their initial recruitment. To address these issues, we used long-term, live confocal imaging of presynaptic terminal formation in cultured cortical neurons after contact with the synaptogenic postsynaptic adhesion proteins neuroligin-1 or SynCAM-1. Surprisingly, we find that trans-synaptic adhesion does not attract SV or AZ proteins nor alter their transport. In addition, although neurexin (the presynap...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bc23bd66cfcd199b6961f55a586cc156" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":76908007,"asset_id":65207376,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/76908007/download_file?st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&st=MTczMjQzNDIwNiw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="65207376"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="65207376"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 65207376; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=65207376]").text(description); $(".js-view-count[data-work-id=65207376]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 65207376; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='65207376']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 65207376, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "bc23bd66cfcd199b6961f55a586cc156" } } $('.js-work-strip[data-work-id=65207376]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":65207376,"title":"Dynamic mechanisms of neuroligin-dependent presynaptic terminal assembly in living cortical neurons","translated_title":"","metadata":{"abstract":"Synapse formation occurs when synaptogenic signals trigger coordinated development of pre and postsynaptic structures. One of the best-characterized synaptogenic signals is trans-synaptic adhesion. However, it remains unclear how synaptic proteins are recruited to sites of adhesion. In particular, it is unknown whether synaptogenic signals attract synaptic vesicle (SV) and active zone (AZ) proteins to nascent synapses or instead predominantly function to create sites that are capable of forming synapses. It is also unclear how labile synaptic proteins are at developing synapses after their initial recruitment. To address these issues, we used long-term, live confocal imaging of presynaptic terminal formation in cultured cortical neurons after contact with the synaptogenic postsynaptic adhesion proteins neuroligin-1 or SynCAM-1. Surprisingly, we find that trans-synaptic adhesion does not attract SV or AZ proteins nor alter their transport. In addition, although neurexin (the presynap...","publication_date":{"day":29,"month":1,"year":2014,"errors":{}},"publication_name":"Neural development"},"translated_abstract":"Synapse formation occurs when synaptogenic signals trigger coordinated development of pre and postsynaptic structures. One of the best-characterized synaptogenic signals is trans-synaptic adhesion. However, it remains unclear how synaptic proteins are recruited to sites of adhesion. In particular, it is unknown whether synaptogenic signals attract synaptic vesicle (SV) and active zone (AZ) proteins to nascent synapses or instead predominantly function to create sites that are capable of forming synapses. It is also unclear how labile synaptic proteins are at developing synapses after their initial recruitment. To address these issues, we used long-term, live confocal imaging of presynaptic terminal formation in cultured cortical neurons after contact with the synaptogenic postsynaptic adhesion proteins neuroligin-1 or SynCAM-1. Surprisingly, we find that trans-synaptic adhesion does not attract SV or AZ proteins nor alter their transport. 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