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type="text/javascript" src="https://d1bxh8uas1mnw7.cloudfront.net/assets/embed.js"></script> <p class="article-title" style="-webkit-font-smoothing: antialiased; margin: 0px 0px 7px; padding: 0px; border: 0px; outline: 0px; vertical-align: baseline; font-variant-numeric: inherit; font-variant-east-asian: inherit; font-variant-alternates: inherit; font-stretch: inherit; font-size: 22px; line-height: 28px; font-family: "Helvetica Neue", Helvetica, Arial, sans-serif; font-optical-sizing: inherit; font-kerning: inherit; font-feature-settings: inherit; font-variation-settings: inherit; color: rgb(0, 0, 0);"> </p> <div class="row"> <div class="left" style="float:left;padding:10px;height:100%;"> <div class="fixed-menu"> <p><strong><a href="#research_spotlight">Research Spotlight</a></strong></p> <p><strong><a href="#most_discussed">Most Discussed</a></strong></p> </div> </div> <div class="right" style="padding-left:0px;padding-top:0px;float:left;height:100%;"> <h2 class="section-head"><a name="research_spotlight"></a> Research Spotlight</h2> <div class="item-box"><!--SPOTLIGHT ARTICLE #1--> <div class="discussed-article"> <p class="article-title"><a href="https://doi.org/10.1523/JNEUROSCI.1191-24.2024">Breathing Modulates Network Activity in Frontal Brain Regions During Anxiety</a></p> </div> </div> <div class="item-box"> <div class="discussed-article"> <p class="article-author rightbadge-author"><em>Ana Luiza Alves Dias, Davi Carvalho Drieskens, Joseph Andrews Belo, Elis H. Duarte, Diego Laplagne, and Adriano B. L. Tort</em></p> <p class="sig-stmt">When a person experiences anxiety, their breathing patterns quicken. Understanding how breathing impacts neural activity during anxiety could lead to new anxiety treatment interventions targeting respiratory control. Adriano Tort from the Federal University of Rio Grande do Norte led a study exploring the interplay between anxiety, breathing patterns, and brain activity in rats. The researchers discovered that accelerated breathing from anxiety triggers oscillatory neural activity in frontal brain regions that contribute to emotional processing. The frequency of these neural oscillations varied depending on breathing patterns. These findings may pave the way for further research on how breathing influences brain function during emotional states.</p> </div> </div> <svg height="3px" width="100%"> <line style="stroke:rgb(211,211,211);stroke-width:3" x1="7.5%" x2="92.5%"></line> </svg> <div class="item-box"><!--SPOTLIGHT ARTICLE #2--> <div class="discussed-article"> <p class="article-title"><a href="https://doi.org/10.1523/JNEUROSCI.0080-24.2024">Computational and Neural Evidence for Altered Fast and Slow Learning from Losses in Problem Gambling</a></p> </div> </div> <div class="item-box"> <div class="discussed-article"> <p class="article-author rightbadge-author"><em>Kiyohito Iigaya, Tobias Larsen, Tim Fong, and John P. O’Doherty </em></p> <p class="sig-stmt">Millions of people in America suffer from problematic gambling issues. Kiyohito Iigaya from Columbia University led a study to explore why people who engage in problematic gambling continue gambling despite repeated losses that worsen their quality of life. The researchers used a decision-making task to probe behavior related to reward learning and aversion to loss as they imaged the brains of study participants. This methodology revealed that problem gamblers are less able to adjust their predictions following losses as compared with people who recreationally gamble. According to the researchers, this may be because people who gamble problematically rely more on long-term learning, over the course of years, and are less able to learn from the losses in their immediate pasts. Neuroimaging revealed three brain regions that may contribute to this learning disparity, pointing to potential targets for problematic gambling treatment.</p> </div> </div> <svg height="3px" width="100%"> <line style="stroke:rgb(211,211,211);stroke-width:3" x1="7.5%" x2="92.5%"></line> </svg> <div class="item-box"><!--SPOTLIGHT ARTICLE #3--> <div class="discussed-article"> <p class="article-title"><a href="https://www.jneurosci.org/content/44/33/e1195232024">Symmetry in Frontal But Not Motor and Somatosensory Cortical Projections</a></p> </div> </div> <div class="item-box"> <div class="discussed-article"> <p class="article-author rightbadge-author"><em>Andrew E. Papale, Madhumita Harish, Ronald F. Paletzki, Nathan J. O’Connor, Brian S. Eastwood, Rebecca P. Seal, Ross S. Williamson, Charles R. Gerfen, and Bryan M. Hooks</em></p> <p class="sig-stmt">Papale and colleagues mapped out connections between neurons that form the cellular basis of coordinated movement planning across the two hemispheres of the frontal cortex. Unlike projections from sensory and motor areas of the cerebral cortex, projections from the frontal cortex in mice make strong, symmetrical connections to the cortex and basal ganglia in the opposite hemisphere, suggesting that such connectivity plays an important role in achieving unified, coordinated motor actions. Strong structural symmetry in neural pathways for motor planning may enable better movement integration between the two sides of the body. Because the frontal cortex has two hemispheres, but individuals generally feel a single consciousness supporting voluntary choices, such symmetrical connectivity may be significant in achieving a unified sense of self. Extending this study to primates and humans, who have a much expanded and complicated frontal cortex, may help address how evaluating the value of potential choices in two hemispheres can be integrated into a single choice for an individual (and how this might go awry in disease states).</p> </div> </div> <svg height="3px" width="100%"> <line style="stroke:rgb(211,211,211);stroke-width:3" x1="7.5%" x2="92.5%"></line> </svg> <div class="item-box"><!--SPOTLIGHT ARTICLE #4--> <div class="discussed-article"> <p class="article-title"><a href="https://www.jneurosci.org/content/44/36/e0301242024">Distinct Neural Plasticity Enhancing Visual Perception</a></p> </div> </div> <div class="item-box"> <div class="discussed-article"> <p class="article-author rightbadge-author"><em>Taly Kondat, Niv Tik, Haggai Sharon, Ido Tavor, and Nitzan Censor</em></p> <p class="sig-stmt">Kondat and colleagues identified a novel neural pathway in the human brain supporting enhanced perceptual learning efficiency. This unique pathway is triggered by brief memory reactivations instead of prolonged repetition-based practice, while yielding similar remarkable learning gains. The brain recruits higher-order control and attentional resources to enable this novel form of learning, which is further supported by changes in inter-regional functional brain connectivity.</p> </div> </div> <h2 class="section-head" style="margin-top:30px;"><a name="most_discussed"></a> Most-Discussed Research Published in October</h2> <p class="intro-text">Below are five Early Release articles that generated the most online discussion in October 2024, as measured by Altmetric. Altmetric data is available for all articles published in JNeurosci on the Info & Metrics tab. Learn more about how the Altmetric score is calculated.</p> <div class="item-box"><!-- FEATURED ARTICLE #1 --> <div class="altmetric-embed alt-badge leftbadge" data-badge-details="none" data-badge-popover="top" data-badge-type="medium-donut" data-doi="https://doi.org/10.1523/JNEUROSCI.0374-24.2024"> </div> <div class="discussed-article"> <p class="article-title"><a href="https://www.jneurosci.org/content/early/2024/10/18/JNEUROSCI.0374-24.2024?utm_source=JN&utm_medium=Webpage&utm_campaign=Most_Discussed">The spatiotemporal dynamics of bottom-up and top-down processing during at-a-glance reading</a></p> <p class="article-author leftbadge-author"><em>Nigel Flower and Liina Pylkkänen</em></p> <p class="sig-stmt">Language processing, like all cognitive domains, is profoundly influenced by top-down knowledge. One type of evidence of this is oversight of errors in the signal. For example, in sentence comprehension, individuals often fail to detect word order errors, such as transposed words mid-sentence. Utilizing rapid parallel visual presentation (RPVP), we investigated this phenomenon by exposing participants to four-word sentences for 300ms. Magnetoencephalography revealed robust differentiation between grammatical and reversed sentences in left lateral language cortex starting at 213ms post-presentation. Intriguingly, initial neural responses to inner transpositions treated them as deviant, but 100ms later, neural signals grouped them with grammatical sentence, indicating rapid error correction. These findings reveal the brain's remarkable capacity to reconcile bottom-up input with linguistic knowledge almost instantaneously.</p> </div> </div> <svg height="3px" width="100%"> <line style="stroke:rgb(211,211,211);stroke-width:3" x1="7.5%" x2="92.5%"></line> </svg> <div class="item-box"><!-- FEATURED ARTICLE #2 --> <div class="altmetric-embed alt-badge rightbadge" data-badge-details="none" data-badge-popover="top" data-badge-type="medium-donut" data-doi="https://doi.org/10.1523/JNEUROSCI.0142-23.2024"> </div> <div class="discussed-article"> <p class="article-title"><a href="https://www.jneurosci.org/content/early/2024/09/29/JNEUROSCI.0142-23.2024?utm_source=JN&utm_medium=Webpage&utm_campaign=Most_Discussed">Neural predictors of fear depend on the situation</a></p> <p class="article-author rightbadge-author"><em>Yiyu Wang, Philip Kragel, and Ajay B. Satpute</em></p> <p class="sig-stmt">Much of the debate on the nature of emotion concerns the uniformity or heterogeneity of representation for particular emotion categories. Here we provide evidence that widely distributed activation patterns characteristic of recent neural signatures of fear reflect an amalgam of functionally heterogeneous brain states. Participants completed a novel fMRI task that parametrically examined subjective fear within and across three content-rich and naturalistic situations: fear of heights, spiders, and social threats. Using searchlight analysis and machine learning methods, we show that the overwhelming majority of brain regions that predict fear only do so for certain situations. These findings carry implications for the generalization of findings on fear across species, translational models of fear and anxiety, and developing neural signatures of fear.</p> </div> </div> <svg height="3px" width="100%"> <line style="stroke:rgb(211,211,211);stroke-width:3" x1="7.5%" x2="92.5%"></line> </svg> <div class="item-box"><!-- FEATURED ARTICLE #3 --> <div class="altmetric-embed alt-badge leftbadge" data-badge-details="none" data-badge-popover="top" data-badge-type="medium-donut" data-doi="https://doi.org/10.1523/JNEUROSCI.0805-24.2024"> </div> <div class="discussed-article"> <p class="article-title"><a href="https://www.jneurosci.org/content/early/2024/10/08/JNEUROSCI.0805-24.2024?utm_source=JN&utm_medium=Webpage&utm_campaign=Most_Discussed">Developmental spike timing-dependent long-term depression requires astrocyte D-serine at L2/3-L2/3 synapses of the mouse somatosensory cortex</a></p> <p class="article-author rightbadge-author"><em>Yuniesky Andrade-Talavera, Joaquín Sánchez-Gómez, Heriberto Coatl-Cuaya, and Antonio Rodríguez-Moreno</em></p> <p class="sig-stmt">We show here the mechanisms and role of astrocytes and gliotransmitters in a postsynaptic spike timing dependent long-term depression (t-LTD) form defined at layer (L)2/3-L2/3 synapses of the somatosensory cortex. We have discovered that this form of plasticity involves N-methyl D-aspartate receptors (NMDAR) containing the GluN2B subunit and requires astrocytes and the gliotransmitter D-serine to co-activate (together with glutamate) postsynaptic NMDAR to mediate LTD. This can be a general mechanism in the brain to define different forms of plasticity. Defining the mechanisms of synaptic plasticity may have important implications for brain repair, sensorial recovery, the treatment of neurodevelopmental disorders and even, for educational policy.</p> </div> </div> <div class="item-box"><!-- FEATURED ARTICLE #4 --> <div class="altmetric-embed alt-badge rightbadge" data-badge-details="none" data-badge-popover="top" data-badge-type="medium-donut" data-doi="https://doi.org/10.1523/JNEUROSCI.0013-24.2024"> </div> <div class="discussed-article"> <p class="article-title"><a href="https://doi.org/10.1523/JNEUROSCI.0013-24.2024?utm_source=JN&utm_medium=Webpage&utm_campaign=Most_Discussed">Orbitofrontal cortex mediates sustained basolateral amygdala encoding of cued reward seeking states</a></p> <p class="article-author leftbadge-author"><em>David J. Ottenheimer, Katherine R. Vitale, Frederic Ambroggi, Patricia H. Janak, and Benjamin T. Saunders</em></p> <p class="sig-stmt">Appropriate representation of the current need for motivated reward seeking, especially under situations of uncertainty or ambiguity, is critical for adaptive behavior. Here, we recorded activity of neurons in the basolateral amygdala (BLA) in rats during conditioned reward seeking, finding a sustained cue-evoked population-level code, which terminated once reward was received. Inactivation of a major BLA input, the orbitofrontal cortex (OFC), blunted sustained cue-evoked activity in BLA and reduced reward seeking. Optogenetic disruption of BLA activity and OFC terminals in BLA also reduced reward seeking. Together, these results show that the BLA represents conditioned motivational states with sustained neural activity - this signal is critical for cue-invigorated reward seeking and depends on functional input from the orbitofrontal cortex.</p> </div> </div> <svg height="3px" width="100%"> <line style="stroke:rgb(211,211,211);stroke-width:3" x1="7.5%" x2="92.5%"></line> </svg> <div class="item-box"><!-- FEATURED ARTICLE #5 --> <div class="altmetric-embed alt-badge leftbadge" data-badge-details="none" data-badge-popover="top" data-badge-type="medium-donut" data-doi="https://doi.org/10.1523/JNEUROSCI.0938-24.2024"> </div> <div class="discussed-article"> <p class="article-title"><a href="https://doi.org/10.1523/JNEUROSCI.0938-24.2024?utm_source=JN&utm_medium=Webpage&utm_campaign=Most_Discussed">Monocyte invasion into the retina restricts the regeneration of neurons from Müller glia</a></p> <p class="article-author leftbadge-author"><em>Nicolai Blasdel, Sucheta Bhattacharya, Phoebe C. Donaldson, Thomas A. Reh, and Levi Todd</em></p> <p class="sig-stmt">Regeneration of neurons in the central nervous system is extremely limited in mammals. Transgenic overexpression of the proneural transcription factor Ascl1 enables mammalian retinal glia to regenerate some neurons lost to injury. We found that during this regenerative response to injury, monocytes from the periphery invade the neural retina and these inflammatory cells negatively regulate the ability of Müller glia to reprogram into neurogenic progenitors. When monocytes are inhibited from infiltrating the retina, regeneration of neurons from Müller glia is significantly enhanced. 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