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(PDF) Water deprivation activates a glutamatergic projection from the hypothalamic paraventricular nucleus to the rostral ventrolateral medulla
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</script> <script type="application/ld+json">{"@context":"https://schema.org","@type":"ScholarlyArticle","author":[{"@context":"https://schema.org","@type":"Person","name":"Johnny Simmons","url":"https://independent.academia.edu/JohnnySimmons3"},{"@context":"https://schema.org","@type":"Person","name":"Ruth Stornetta","url":"https://virginia.academia.edu/RuthStornetta"}],"contributor":[{"@context":"https://schema.org","@type":"Person","name":"Ruth Stornetta","url":"https://virginia.academia.edu/RuthStornetta"}],"dateCreated":"2016-12-22","datePublished":"2006-01-01","headline":"Water deprivation activates a glutamatergic projection from the hypothalamic paraventricular nucleus to the rostral ventrolateral medulla","image":"https://attachments.academia-assets.com/51025463/thumbnails/1.jpg","inLanguage":"en","keywords":["Zoology","Animals","Male","The","Medical Physiology","Neurons","Paraventricular Nucleus","Tyrosine Hydroxylase","Rats","Sympathetic Nervous System","Neural 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"https://www.academia.edu/login?post_login_redirect_url=https%3A%2F%2Fwww.academia.edu%2F30582769%2FWater_deprivation_activates_a_glutamatergic_projection_from_the_hypothalamic_paraventricular_nucleus_to_the_rostral_ventrolateral_medulla%3Fshow_translation%3Dtrue"; window.loswp.previewableAttachments = [{"id":51025463,"identifier":"Attachment_51025463","shouldShowBulkDownload":false}]; window.loswp.shouldDetectTimezone = true; window.loswp.shouldShowBulkDownload = true; window.loswp.showSignupCaptcha = false window.loswp.willEdgeCache = false; window.loswp.work = {"work":{"id":30582769,"created_at":"2016-12-22T23:39:51.497-08:00","from_world_paper_id":159936031,"updated_at":"2024-11-17T03:29:00.915-08:00","_data":{"grobid_abstract":"Elevated sympathetic outflow contributes to the maintenance of blood pressure in water-deprived rats. The neural circuitry underlying this response may involve activation of a pathway from the hypothalamic paraventricular nucleus (PVH) to the rostral ventrolateral medulla (RVLM). We sought to determine whether the PVH-RVLM projection activated by water deprivation is glutamatergic and/or contains vasopressin-or oxytocin-neurophysins. Vesicular glutamate transporter2 (VGLUT2) mRNA was detected by in situ hybridization in the majority of PVH neurons retrogradely labeled from the ipsilateral RVLM with cholera-toxin subunit B (CTB; 85% on average with regional differences). Very few RVLM-projecting PVH neurons were immunoreactive for oxytocin-or vasopressin-associated neurophysin. Injection of biotinylated dextran amine (BDA) into the PVH produced clusters of BDA-positive nerve terminals within the ipsilateral RVLM that were immunoreactive (ir) for the VGLUT2 protein. Some of these terminals made close appositions with tyrosine-hydroxylase-ir dendrites (presumptive C1 cells). In waterdeprived rats (n=4), numerous VGLUT2 mRNA-positive PVH neurons retrogradely labeled from the ipsilateral RVLM with CTB were c-Fos-ir (16-40% depending on PVH region). In marked contrast, few glutamatergic, RVLM-projecting PVH neurons were c-Fos-ir in control rats (n=3; 0-3% depending on PVH region). Most (94 ± 4%) RVLM-projecting PVH neurons activated by water deprivation contained VGLUT2 mRNA. In summary, the majority of PVH neurons that innervate the RVLM are glutamatergic and this population includes the neurons that are activated by water deprivation. One mechanism by which water deprivation may increase the sympathetic outflow is the activation of a glutamatergic pathway from the PVH to the RVLM.","publication_date":"2006,,","publication_name":"The Journal of Comparative Neurology","grobid_abstract_attachment_id":"51025463"},"document_type":"paper","pre_hit_view_count_baseline":null,"quality":"high","language":"en","title":"Water deprivation activates a glutamatergic projection from the hypothalamic paraventricular nucleus to the rostral ventrolateral medulla","broadcastable":true,"draft":null,"has_indexable_attachment":true,"indexable":true}}["work"]; window.loswp.workCoauthors = [57481840,58281155]; window.loswp.locale = "en"; window.loswp.countryCode = "SG"; window.loswp.cwvAbTestBucket = ""; window.loswp.designVariant = "ds_vanilla"; window.loswp.fullPageMobileSutdModalVariant = "full_page_mobile_sutd_modal"; window.loswp.useOptimizedScribd4genScript = false; window.loginModal = {}; window.loginModal.appleClientId = 'edu.academia.applesignon'; 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if (!viewCountBody) { throw new Error('Failed to find work views element'); } viewCountBody.textContent = `${commaizedViewCount} views`; } catch (error) { // Remove the whole views element if there was some issue parsing. document.getElementById('work-metadata-view-count')?.parentNode?.remove(); throw new Error(`Failed to parse view count: ${viewCount}`, error); } }; // If the DOM is still loading, wait for it to be ready before updating the view count. if (document.readyState === "loading") { document.addEventListener('DOMContentLoaded', () => { updateViewCount(viewCount); }); // Otherwise, just update it immediately. } else { updateViewCount(viewCount); } })();</script></div><p class="ds-work-card--work-abstract ds-work-card--detail ds2-5-body-md">Elevated sympathetic outflow contributes to the maintenance of blood pressure in water-deprived rats. The neural circuitry underlying this response may involve activation of a pathway from the hypothalamic paraventricular nucleus (PVH) to the rostral ventrolateral medulla (RVLM). We sought to determine whether the PVH-RVLM projection activated by water deprivation is glutamatergic and/or contains vasopressin-or oxytocin-neurophysins. Vesicular glutamate transporter2 (VGLUT2) mRNA was detected by in situ hybridization in the majority of PVH neurons retrogradely labeled from the ipsilateral RVLM with cholera-toxin subunit B (CTB; 85% on average with regional differences). Very few RVLM-projecting PVH neurons were immunoreactive for oxytocin-or vasopressin-associated neurophysin. Injection of biotinylated dextran amine (BDA) into the PVH produced clusters of BDA-positive nerve terminals within the ipsilateral RVLM that were immunoreactive (ir) for the VGLUT2 protein. Some of these terminals made close appositions with tyrosine-hydroxylase-ir dendrites (presumptive C1 cells). In waterdeprived rats (n=4), numerous VGLUT2 mRNA-positive PVH neurons retrogradely labeled from the ipsilateral RVLM with CTB were c-Fos-ir (16-40% depending on PVH region). In marked contrast, few glutamatergic, RVLM-projecting PVH neurons were c-Fos-ir in control rats (n=3; 0-3% depending on PVH region). Most (94 ± 4%) RVLM-projecting PVH neurons activated by water deprivation contained VGLUT2 mRNA. In summary, the majority of PVH neurons that innervate the RVLM are glutamatergic and this population includes the neurons that are activated by water deprivation. One mechanism by which water deprivation may increase the sympathetic outflow is the activation of a glutamatergic pathway from the PVH to the RVLM.</p><div class="ds-work-card--button-container"><button class="ds2-5-button js-swp-download-button" data-signup-modal="{"location":"continue-reading-button--work-card","attachmentId":51025463,"attachmentType":"pdf","workUrl":"https://www.academia.edu/30582769/Water_deprivation_activates_a_glutamatergic_projection_from_the_hypothalamic_paraventricular_nucleus_to_the_rostral_ventrolateral_medulla"}">See full PDF</button><button class="ds2-5-button ds2-5-button--secondary js-swp-download-button" data-signup-modal="{"location":"download-pdf-button--work-card","attachmentId":51025463,"attachmentType":"pdf","workUrl":"https://www.academia.edu/30582769/Water_deprivation_activates_a_glutamatergic_projection_from_the_hypothalamic_paraventricular_nucleus_to_the_rostral_ventrolateral_medulla"}"><span class="material-symbols-outlined" style="font-size: 20px" translate="no">download</span>Download PDF</button></div><div class="ds-signup-banner-trigger-container"><div class="ds-signup-banner-trigger ds-signup-banner-trigger-control"></div></div><div class="ds-signup-banner ds-signup-banner-control"><div id="ds-signup-banner-close-button"><button class="ds2-5-button ds2-5-button--secondary ds2-5-button--inverse"><span class="material-symbols-outlined" style="font-size: 20px" translate="no">close</span></button></div><div class="ds-signup-banner-ctas"><img src="//a.academia-assets.com/images/academia-logo-capital-white.svg" /><h4 class="ds2-5-heading-serif-sm">Sign up for access to the world's latest research</h4><button class="ds2-5-button ds2-5-button--inverse ds2-5-button--full-width js-swp-download-button" data-signup-modal="{"location":"signup-banner"}">Sign up for free<span class="material-symbols-outlined" style="font-size: 20px" translate="no">arrow_forward</span></button></div><div class="ds-signup-banner-divider"></div><div class="ds-signup-banner-reasons"><div class="ds-signup-banner-reasons-item"><span class="material-symbols-outlined" style="font-size: 24px" translate="no">check</span><span>Get notified about relevant papers</span></div><div class="ds-signup-banner-reasons-item"><span class="material-symbols-outlined" style="font-size: 24px" translate="no">check</span><span>Save papers to use in your research</span></div><div class="ds-signup-banner-reasons-item"><span class="material-symbols-outlined" style="font-size: 24px" translate="no">check</span><span>Join the discussion with peers</span></div><div class="ds-signup-banner-reasons-item"><span class="material-symbols-outlined" style="font-size: 24px" translate="no">check</span><span>Track your impact</span></div></div></div><script>(() => { // Set up signup banner show/hide behavior: // 1. 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Water deprivation reduced basal CRH mRNA levels but the increments following 4 h of restraint or 6 h lipopolysaccharide (LPS) injection were similar to those in controls. In contrast, water deprivation had no effect on basal VP heteronuclear RNA (hnRNA) and mRNA levels in parvocellular neurons, but responses to restraint or LPS injection were reduced. VP expression in magnocellular paraventricular and supraoptic nuclei, and plasma sodium and vasopressin were higher in water-deprived rats, changes which were unaffected by restraint. LPS injection reduced VP mRNA but not hnRNA levels in magnocellular neurons and increased plasma vasopressin levels only in water-deprived rats independently of changes in plasma sodium. This was accompanied by an increase in vasopressin mRNA content in the posterior pituitary. The data show that the blunted ACTH responses to acute stress during chronic osmotic stimulation are correlated with the inability of parvocellular neurons to increase VP rather than CRH expression. In addition, LPS-induced endotoxemia causes disturbances of the magnocellular vasopressinergic system with an unexpected potentiation of osmotic simulated VP secretion. The lack of increase in VP transcription after LPS and changes in VP mRNA distribution suggest that endotoxemia affect the secretory process at the levels of the neurohypophyseal axon terminal.</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Hypothalamic Pituitary Adrenal Axis and Hypothalamic–Neurohypophyseal Responsiveness in Water-Deprived Rats","attachmentId":43117056,"attachmentType":"pdf","work_url":"https://www.academia.edu/22497152/Hypothalamic_Pituitary_Adrenal_Axis_and_Hypothalamic_Neurohypophyseal_Responsiveness_in_Water_Deprived_Rats","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/22497152/Hypothalamic_Pituitary_Adrenal_Axis_and_Hypothalamic_Neurohypophyseal_Responsiveness_in_Water_Deprived_Rats"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="1" data-entity-id="29624634" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/29624634/Autonomic_Neuroscience_Paraventricular_nucleus_influence_on_renal_sympathetic_activity_in_vasopressin_gene_deleted_rats">Autonomic Neuroscience: Paraventricular nucleus influence on renal sympathetic activity in vasopressin gene-deleted rats</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="33304280" href="https://bham.academia.edu/JohnCoote">John Coote</a></div><p class="ds-related-work--metadata ds2-5-body-xs">Experimental Physiology, 2007</p><p class="ds-related-work--abstract ds2-5-body-sm">In Wistar rats, an increase in renal sympathetic activity is induced by activation of presympathetic neurones in the paraventricular nucleus (PVN) and reflexly by a mild venous haemorrhage. Both stimuli are dependent on the release of vasopressin and glutamate at spinal synapses. The significance of the supraspinal pathway and the co-operative interaction of vasopressin with an excitatory amino acid is unclear. The present study examines this in Brattleboro rats, which have a natural vasopressin gene deletion. The responses were compared with Long-Evans rats, from which Brattleboro rats are derived. All rats were anaesthetized with a mixture of urethane (650 mg kg −1 I.V.) and chloralose (50 mg kg −1 I.V.). Recordings were made of blood pressure, heart rate and renal sympathetic nerve activity (RSNA). Microinjection of D,L-homocysteic acid (DLH, 0.2 M, 100 nl) at sites restricted to the PVN elicited significant increases in RSNA (P < 0.001) in both strains of rats. These changes were significantly reduced (P < 0.01) in Long-Evans rats by intrathecal application to the spinal cord of either a V 1a antagonist or a glutamate antagonist (kynurenic acid), whereas in Brattleboro rats the changes were significantly reduced (P < 0.05) only by kynurenic acid. Removal of 1 ml of venous blood in Long-Evans rats increased RSNA by 28 ± 4% (P < 0.01), which was significantly reduced (P < 0.05) by prior intrathecal application of either the V 1a antagonist or by kynurenic acid. The same test in Brattleboro rats caused a significanty greater (P < 0.05) increase (63 ± 14.7%) in RSNA which, in contrast to Long-Evans rats, was unchanged by intrathecal application of the V 1a antagonist, being significantly reduced (P < 0.01) only by intrathecal kynurenic acid. Thus, in Brattleboro rats, the lack of vasopressin in the brain sympathetic pathways appears to be compensated, acutely, by glutamate-releasing pathways. This might indicate that, in normal rats, vasopressin is more important in maintaining longer term adjustments to stressors.</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Autonomic Neuroscience: Paraventricular nucleus influence on renal sympathetic activity in vasopressin gene-deleted rats","attachmentId":50063458,"attachmentType":"pdf","work_url":"https://www.academia.edu/29624634/Autonomic_Neuroscience_Paraventricular_nucleus_influence_on_renal_sympathetic_activity_in_vasopressin_gene_deleted_rats","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/29624634/Autonomic_Neuroscience_Paraventricular_nucleus_influence_on_renal_sympathetic_activity_in_vasopressin_gene_deleted_rats"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="2" data-entity-id="97814325" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/97814325/The_influence_of_salt_loading_on_vasopressin_gene_expression_in_magno_and_parvocellular_hypothalamic_neurons_An_immunocytochemical_andin_situ_hybridization_analysis">The influence of salt loading on vasopressin gene expression in magno- and parvocellular hypothalamic neurons: An immunocytochemical andin situ hybridization analysis</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="31801985" href="https://independent.academia.edu/GNilaver">G. Nilaver</a></div><p class="ds-related-work--metadata ds2-5-body-xs">Neuroscience, 1999</p><p class="ds-related-work--abstract ds2-5-body-sm">Arginine vasopressin peptide and messenger RNA expression were examined at the cellular level in the magnocellular and parvocellular neurons in the rat paraventricular nucleus after dehydration and rehydration, employing immunocytochemistry and in situ hybridization histochemistry on the same tissue sections. Most magnocellular vasopressinergic neurons of control animals expressed both vasopressin-like immunoreactivity and messenger RNA. However, neurons negative for vasopressin-like immunoreactivity but expressing messenger RNA were also detected, and their number increased during dehydration. In contrast, almost all of the parvocellular vasopressinergic neurons of dehydrated animals expressed vasopressin messenger RNA alone, with continued increase in their number after rehydration, despite return of the number of magnocellular vasopressinergic neurons to the control level. Vasopressin messenger RNA and corticotropin releasing factor-like immunoreactivity were co-localized in the same parvocellular neurons, and vasopressin-immunoreactive nerve terminals were detected in the external zone of the median eminence. These findings suggest that magno-and parvocellular vasopressinergic neurons are differentially activated during dehydration/rehydration. Osmotic stimuli activate all magnocellular vasopressinergic neurons, but the effect is not simultaneous in all of these neurons. Parvocellular vasopressinergic neurons are also activated by the stress of dehydration which effect appears to last longer than in the magnocellular system.</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"The influence of salt loading on vasopressin gene expression in magno- and parvocellular hypothalamic neurons: An immunocytochemical andin situ hybridization analysis","attachmentId":99335087,"attachmentType":"pdf","work_url":"https://www.academia.edu/97814325/The_influence_of_salt_loading_on_vasopressin_gene_expression_in_magno_and_parvocellular_hypothalamic_neurons_An_immunocytochemical_andin_situ_hybridization_analysis","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/97814325/The_influence_of_salt_loading_on_vasopressin_gene_expression_in_magno_and_parvocellular_hypothalamic_neurons_An_immunocytochemical_andin_situ_hybridization_analysis"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="3" data-entity-id="99873450" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/99873450/Switching_control_of_sympathetic_activity_from_forebrain_to_hindbrain_in_chronic_dehydration">Switching control of sympathetic activity from forebrain to hindbrain in chronic dehydration</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="255503957" href="https://independent.academia.edu/EduardoColombari">Eduardo Colombari</a></div><p class="ds-related-work--metadata ds2-5-body-xs">The Journal of physiology, 2011</p><p class="ds-related-work--abstract ds2-5-body-sm">We investigated the mechanisms responsible for increased blood pressure and sympathetic nerve activity (SNA) caused by 2-3 days dehydration (DH) both in vivo and in situ preparations. In euhydrated (EH) rats, systemic application of the AT(1) receptor antagonist Losartan and subsequent pre-collicular transection (to remove the hypothalamus) significantly reduced thoracic (t)SNA. In contrast, in DH rats, Losartan, followed by pre-collicular and pontine transections, failed to reduce tSNA, whereas transection at the medulla-spinal cord junction massively reduced tSNA. In DH but not EH rats, selective inhibition of the commissural nucleus tractus solitarii (cNTS) significantly reduced tSNA. Comparable data were obtained in both in situ and in vivo (anaesthetized/conscious) rats and suggest that following chronic dehydration, the control of tSNA transfers from supra-brainstem structures (e.g. hypothalamus) to the medulla oblongata, particularly the cNTS. As microarray analysis revealed ...</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Switching control of sympathetic activity from forebrain to hindbrain in chronic dehydration","attachmentId":100846257,"attachmentType":"pdf","work_url":"https://www.academia.edu/99873450/Switching_control_of_sympathetic_activity_from_forebrain_to_hindbrain_in_chronic_dehydration","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/99873450/Switching_control_of_sympathetic_activity_from_forebrain_to_hindbrain_in_chronic_dehydration"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="4" data-entity-id="22543807" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/22543807/Colocalization_of_vasopressin_and_oxytocin_in_hypothalamic_magnocellular_neurons_in_water_deprived_rats">Colocalization of vasopressin and oxytocin in hypothalamic magnocellular neurons in water-deprived rats</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="44022464" href="https://independent.academia.edu/ValeryGrinevich">Valery Grinevich</a></div><p class="ds-related-work--metadata ds2-5-body-xs">Neuropeptides, 2001</p><p class="ds-related-work--abstract ds2-5-body-sm">The posterior lobe hormones vasopressin and oxytocin are expressed in mutually-exclusive sets of magnocellular hypothamalic neurons. However, under certain functional conditions a partial coexpression has been observed. In the present study we subjected adult rats to long-term osmotic stress by water deprivation for up to 3 days. After 3 days, a marked reduction of vasopressin immunostaining was observed in the paraventricular and supraoptic nuclei as compared with controls. Coexistence of oxytocin and vasopressin occurred in a portion of the magnocellular neurons. Many fibers of the hypothalamio-neurohypophyseal tract contained both peptides. Rehydration for 24 h after 3 days of thirsting resulted in a light recovery of vasopressin immunoreactivity with almost no magnocellular neurons containing both nonapeptides. Our findings indicate that magnocellular hypothalamo-neurohypophysial neurons are capable of oxytocin and vasopressin coexpression upon extended osmotic stress. ß</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Colocalization of vasopressin and oxytocin in hypothalamic magnocellular neurons in water-deprived rats","attachmentId":43158632,"attachmentType":"pdf","work_url":"https://www.academia.edu/22543807/Colocalization_of_vasopressin_and_oxytocin_in_hypothalamic_magnocellular_neurons_in_water_deprived_rats","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/22543807/Colocalization_of_vasopressin_and_oxytocin_in_hypothalamic_magnocellular_neurons_in_water_deprived_rats"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="5" data-entity-id="97742652" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/97742652/Salt_induced_sympathoexcitation_involves_vasopressin_V1a_receptor_activation_in_the_paraventricular_nucleus_of_the_hypothalamus">Salt-induced sympathoexcitation involves vasopressin V1a receptor activation in the paraventricular nucleus of the hypothalamus</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="259644584" href="https://independent.academia.edu/NataliaRibeiro130">Natalia Ribeiro</a></div><p class="ds-related-work--metadata ds2-5-body-xs">American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2015</p><p class="ds-related-work--abstract ds2-5-body-sm">A high-salt diet can lead to hydromineral imbalance and increases in plasma sodium and osmolality. It is recognized as one of the major contributing factors for cardiovascular diseases such as hypertension. The paraventricular nucleus (PVN) plays a pivotal role in osmotically driven sympathoexcitation and high blood pressure, the precise mechanisms of which are not fully understood. Recent evidence indicates that AVP released from magnocellular neurons might be involved in this process. Using a combination of in vivo and in situ studies, we sought to investigate whether AVP, acting on PVN neurons, can change mean arterial pressure (MAP) and sympathetic nerve activity (SNA) in euhydrated male rats. Furthermore, we wanted to determine whether V1a receptors on PVN neurons would be involved in salt-induced sympathoexcitation and hypertension. In rats, 4 days of salt loading (NaCl 2%) elicited a significant increase in plasma osmolality (39 ± 7 mosmol/kgH2O), an increase in MAP (26 ± 2 m...</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Salt-induced sympathoexcitation involves vasopressin V1a receptor activation in the paraventricular nucleus of the hypothalamus","attachmentId":99282350,"attachmentType":"pdf","work_url":"https://www.academia.edu/97742652/Salt_induced_sympathoexcitation_involves_vasopressin_V1a_receptor_activation_in_the_paraventricular_nucleus_of_the_hypothalamus","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/97742652/Salt_induced_sympathoexcitation_involves_vasopressin_V1a_receptor_activation_in_the_paraventricular_nucleus_of_the_hypothalamus"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="6" data-entity-id="17870764" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/17870764/Increased_vasopressin_transmission_from_the_paraventricular_nucleus_to_the_rostral_medulla_augments_cardiorespiratory_outflow_in_chronic_intermittent_hypoxia_conditioned_rats">Increased vasopressin transmission from the paraventricular nucleus to the rostral medulla augments cardiorespiratory outflow in chronic intermittent hypoxia-conditioned rats</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="32868221" href="https://case.academia.edu/JosephLamanna">Joseph C LaManna</a></div><p class="ds-related-work--metadata ds2-5-body-xs">The Journal of Physiology, 2010</p><p class="ds-related-work--abstract ds2-5-body-sm">A co-morbidity of sleep apnoea is hypertension associated with elevated sympathetic nerve activity (SNA) which may result from conditioning to chronic intermittent hypoxia (CIH). Our hypothesis is that SNA depends on input to the rostral ventrolateral medulla (RVLM) from neurons in the paraventricular nucleus (PVN) that release arginine vasopressin (AVP) and specifically, that increased SNA evoked by CIH depends on this excitatory input. In two sets of neuroanatomical experiments, we determined if AVP neurons project from the PVN to the RVLM and if arginine vasopressin (V 1A ) receptor expression increases in the RVLM after CIH conditioning (8 h per day for 10 days). In the first set, cholera toxin β subunit (CT-β) was microinjected into the RVLM to retrogradely label the PVN neurons. Immunohistochemical staining demonstrated that 14.6% of CT-β-labelled PVN neurons were double-labelled with AVP. In the second set, sections of the medulla were immunolabelled for V 1A receptors, and the V 1A receptor-expressing cell count was significantly greater in the RVLM (P < 0.01) and in the neighbouring rostral ventral respiratory column (rVRC) from CIH-than from room air (RA)-conditioned rats. In a series of physiological experiments, we determined if blocking V 1A receptors in the medulla would normalize blood pressure in CIH-conditioned animals and attenuate its response to disinhibition of PVN. Blood pressure (BP), heart rate (HR), diaphragm (D EMG ) and genioglossus muscle (GG EMG ) activity were recorded in anaesthetized, ventilated and vagotomized rats. The PVN was disinhibited by microinjecting a GABA A receptor antagonist, bicuculline (BIC, 0.1 nmol), before and after blocking V 1A receptors within the RVLM and rVRC with SR49059 (0.2 nmol). In RA-conditioned rats, disinhibition of the PVN increased BP, HR, minute D EMG and GG EMG activity and these increases were attenuated after blocking V 1A receptors. In CIH-conditioned rats, a significantly greater dose of blocker (0.4 nmol) was required to blunt these physiological responses (P < 0.05). Further, this dose normalized the baseline BP. In summary, AVP released by a subset of PVN neurons modulates cardiorespiratory output via V 1A receptors in the RVLM and rVRC, and increased SNA in CIH-conditioned animals depends on up-regulation of V 1A receptors in the RVLM.</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Increased vasopressin transmission from the paraventricular nucleus to the rostral medulla augments cardiorespiratory outflow in chronic intermittent hypoxia-conditioned rats","attachmentId":39754701,"attachmentType":"pdf","work_url":"https://www.academia.edu/17870764/Increased_vasopressin_transmission_from_the_paraventricular_nucleus_to_the_rostral_medulla_augments_cardiorespiratory_outflow_in_chronic_intermittent_hypoxia_conditioned_rats","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/17870764/Increased_vasopressin_transmission_from_the_paraventricular_nucleus_to_the_rostral_medulla_augments_cardiorespiratory_outflow_in_chronic_intermittent_hypoxia_conditioned_rats"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="7" data-entity-id="30189055" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/30189055/Vesicular_glutamate_transporter_DNPI_VGLUT2_is_expressed_by_both_C1_adrenergic_and_nonaminergic_presympathetic_vasomotor_neurons_of_the_rat_medulla">Vesicular glutamate transporter DNPI/VGLUT2 is expressed by both C1 adrenergic and nonaminergic presympathetic vasomotor neurons of the rat medulla</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="57481840" href="https://virginia.academia.edu/RuthStornetta">Ruth Stornetta</a></div><p class="ds-related-work--metadata ds2-5-body-xs">The Journal of Comparative Neurology, 2002</p><p class="ds-related-work--abstract ds2-5-body-sm">The main source of excitatory drive to the sympathetic preganglionic neurons that control blood pressure is from neurons located in the rostral ventrolateral medulla (RVLM). This monosynaptic input includes adrenergic (C1), peptidergic, and noncatecholaminergic neurons. Some of the cells in this pathway are suspected to be glutamatergic, but conclusive evidence is lacking. In the present study we sought to determine whether these presympathetic neurons express the vesicular glutamate transporter BNPI/VGLUT1 or the closely related gene DNPI, the rat homolog of the mouse vesicular glutamate transporter VGLUT2. Both BNPI/VGLUT1 and DNPI/VGLUT2 mRNAs were detected in the medulla oblongata by in situ hybridization, but only DNPI/VGLUT2 mRNA was present in the RVLM. Moreover, BNPI immunoreactivity was absent from the thoracic spinal cord lateral horn. DNPI/ VGLUT2 mRNA was present in many medullary cells retrogradely labeled with Fluoro-Gold from the spinal cord (T2; four rats). Within the RVLM, 79% of the bulbospinal C1 cells contained DNPI/VGLUT2 mRNA. Bulbospinal noradrenergic A5 neurons did not contain DNPI/VGLUT2 mRNA. The RVLM of six unanesthetized rats subjected to 2 hours of hydralazine-induced hypotension contained tenfold more c-Fos-ir DNPI/VGLUT2 neurons than that of six saline-treated controls. c-Fos-ir DNPI/VGLUT2 neurons included C1 and non-C1 neurons (3:2 ratio). In seven barbiturate-anesthetized rats, 16 vasomotor presympathetic neurons were filled with biotinamide and analyzed for the presence of tyrosine hydroxylase immunoreactivity and/or DNPI/VGLUT2 mRNA. Biotinamide-labeled neurons included C1 and non-C1 cells. Most non-C1 (9/10) and C1 presympathetic cells (5/6) contained DNPI/VGLUT2 mRNA. In conclusion, DNPI/VGLUT2 is expressed by most blood pressureregulating presympathetic cells of the RVLM. The data suggest that these neurons may be glutamatergic and that the C1 adrenergic phenotype is one of several secondary phenotypes that are differentially expressed by subgroups of these cells.</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Vesicular glutamate transporter DNPI/VGLUT2 is expressed by both C1 adrenergic and nonaminergic presympathetic vasomotor neurons of the rat medulla","attachmentId":50648405,"attachmentType":"pdf","work_url":"https://www.academia.edu/30189055/Vesicular_glutamate_transporter_DNPI_VGLUT2_is_expressed_by_both_C1_adrenergic_and_nonaminergic_presympathetic_vasomotor_neurons_of_the_rat_medulla","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/30189055/Vesicular_glutamate_transporter_DNPI_VGLUT2_is_expressed_by_both_C1_adrenergic_and_nonaminergic_presympathetic_vasomotor_neurons_of_the_rat_medulla"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="8" data-entity-id="26946347" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/26946347/Losartan_blocks_the_excitatory_effect_of_peripheral_hypertonic_stimulation_on_vasopressinergic_neurons_in_hypothalamic_paraventricular_nucleus_in_rats_electrophysiological_and_immunocytochemical_evidence">Losartan blocks the excitatory effect of peripheral hypertonic stimulation on vasopressinergic neurons in hypothalamic paraventricular nucleus in rats: electrophysiological and immunocytochemical evidence</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="47361672" href="https://independent.academia.edu/guoshiyu">shiyu guo</a></div><p class="ds-related-work--metadata ds2-5-body-xs">Neuroscience Letters, 2005</p><p class="ds-related-work--abstract ds2-5-body-sm">The effect of peripheral hypertonic stimulation on the neurons of hypothalamic paraventricular nucleus (PVN) was investigated in the present study with both electrophysiological and immunocytochemical methods. The discharge frequency of the neurons with phasic activity in PVN could be increased by intraperitoneal (i.p.) injection of hypertonic saline (HS, 1.5 M NaCl) (from 2.8 ± 0.5 Hz to 5.4 ± 0.9 Hz, P < 0.001). The Fos expression in PVN could be enhanced (from 21.2 ± 12.9 to 217.3 ± 38.5 Fos-positive neurons, P < 0.001) by i.p. HS and the majority of AVP-positive neurons expressing Fos (91.7 ± 3.6%) was in magnocellular subdivision of PVN. After intracerebroventricular (i.c.v.) injection of losartan, angiotensin II type 1 (AT 1 ) receptor antagonist (5 g/l), the excitatory effect of peripheral hypertonic stimulation on PVN neurons with phasic activity was inhibited significantly, and the number of the neurons co-expressing Fos and AVP in PVN decreased significantly (P < 0.001) as well. The result demonstrated that the vasopressinergic neurons in PVN could be excited by peripheral hypertonic stimulation, and this excitation might be mediated by angiotensin II fibers projecting from subfornical organ to PVN.</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Losartan blocks the excitatory effect of peripheral hypertonic stimulation on vasopressinergic neurons in hypothalamic paraventricular nucleus in rats: electrophysiological and immunocytochemical evidence","attachmentId":47210115,"attachmentType":"pdf","work_url":"https://www.academia.edu/26946347/Losartan_blocks_the_excitatory_effect_of_peripheral_hypertonic_stimulation_on_vasopressinergic_neurons_in_hypothalamic_paraventricular_nucleus_in_rats_electrophysiological_and_immunocytochemical_evidence","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/26946347/Losartan_blocks_the_excitatory_effect_of_peripheral_hypertonic_stimulation_on_vasopressinergic_neurons_in_hypothalamic_paraventricular_nucleus_in_rats_electrophysiological_and_immunocytochemical_evidence"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="9" data-entity-id="54422959" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/54422959/Afferent_renal_inputs_to_paraventricular_nucleus_vasopressin_and_oxytocin_neurosecretory_neurons">Afferent renal inputs to paraventricular nucleus vasopressin and oxytocin neurosecretory neurons</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="136741945" href="https://independent.academia.edu/CirielloJohn">John Ciriello</a></div><p class="ds-related-work--metadata ds2-5-body-xs">American Journal of Physiology-Regulatory, Integrative and Comparative Physiology</p><p class="ds-related-work--abstract ds2-5-body-sm">Extracellular single-unit recording experiments were done in pentobarbital sodium-anesthetized rats to investigate the effects of electrical stimulation of afferent renal nerves (ARN) and renal vein (RVO) or artery (RAO) occlusion on the discharge rate of putative arginine vasopressin (AVP) and oxytocin (Oxy) neurons in the paraventricular nucleus of the hypothalamus (PVH). PVH neurons antidromically activated by electrical stimulation of the neurohypophysis were classified as either AVP or Oxy secreting on the basis of their spontaneous discharge patterns and response to activation of arterial baroreceptors. Ninety-eight putative neurosecretory neurons in the PVH were tested for their response to electrical stimulation of ARN: 44 were classified as putative AVP and 54 as putative Oxy neurons. Of the 44 AVP neurons, 52% were excited, 7% were inhibited, and 41% were nonresponsive to ARN stimulation. Of the 54 Oxy neurons, 43% were excited, 6% inhibited, and 51% were not affected by A...</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Afferent renal inputs to paraventricular nucleus vasopressin and oxytocin neurosecretory neurons","attachmentId":70793065,"attachmentType":"pdf","work_url":"https://www.academia.edu/54422959/Afferent_renal_inputs_to_paraventricular_nucleus_vasopressin_and_oxytocin_neurosecretory_neurons","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/54422959/Afferent_renal_inputs_to_paraventricular_nucleus_vasopressin_and_oxytocin_neurosecretory_neurons"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div></div></div><div class="ds-sticky-ctas--wrapper js-loswp-sticky-ctas hidden"><div class="ds-sticky-ctas--grid-container"><div class="ds-sticky-ctas--container"><button class="ds2-5-button js-swp-download-button" data-signup-modal="{"location":"continue-reading-button--sticky-ctas","attachmentId":51025463,"attachmentType":"pdf","workUrl":null}">See full PDF</button><button class="ds2-5-button ds2-5-button--secondary js-swp-download-button" data-signup-modal="{"location":"download-pdf-button--sticky-ctas","attachmentId":51025463,"attachmentType":"pdf","workUrl":null}"><span class="material-symbols-outlined" style="font-size: 20px" translate="no">download</span>Download PDF</button></div></div></div><div class="ds-below-fold--grid-container"><div class="ds-work--container js-loswp-embedded-document"><div class="attachment_preview" data-attachment="Attachment_51025463" style="display: none"><div class="js-scribd-document-container"><div class="scribd--document-loading js-scribd-document-loader" style="display: block;"><img alt="Loading..." src="//a.academia-assets.com/images/loaders/paper-load.gif" /><p>Loading Preview</p></div></div><div style="text-align: center;"><div class="scribd--no-preview-alert js-preview-unavailable"><p>Sorry, preview is currently unavailable. 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