IF 14.7 1区医学

Neuron Pub Date : 2024-09-04 Epub Date: 2024-07-03 DOI: 10.1016/j.neuron.2024.06.007

David C Wang, Fernando Santos-Valencia, Jun H Song, Kevin M Franks, Liqun Luo

{"title":"Embryonically active piriform cortex neurons promote intracortical recurrent connectivity during development.","authors":"David C Wang, Fernando Santos-Valencia, Jun H Song, Kevin M Franks, Liqun Luo","doi":"10.1016/j.neuron.2024.06.007","DOIUrl":"10.1016/j.neuron.2024.06.007","url":null,"abstract":"Neuronal activity plays a critical role in the maturation of circuits that propagate sensory information into the brain. How widely does early activity regulate circuit maturation across the developing brain? Here, we used targeted recombination in active populations (TRAP) to perform a brain-wide survey for prenatally active neurons in mice and identified the piriform cortex as an abundantly TRAPed region. Whole-cell recordings in neonatal slices revealed preferential interconnectivity within embryonically TRAPed piriform neurons and their enhanced synaptic connectivity with other piriform neurons. In vivo Neuropixels recordings in neonates demonstrated that embryonically TRAPed piriform neurons exhibit broad functional connectivity within piriform and lead spontaneous synchronized population activity during a transient neonatal period, when recurrent connectivity is strengthening. Selectively activating or silencing these neurons in neonates enhanced or suppressed recurrent synaptic strength, respectively. Thus, embryonically TRAPed piriform neurons represent an interconnected hub-like population whose activity promotes recurrent connectivity in early development.","PeriodicalId":19313,"journal":{"name":"Neuron","volume":" ","pages":"2938-2954.e6"},"PeriodicalIF":14.7,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11377168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141534948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mentoring to propagate racial inclusivity in neuroscience. 指导宣传神经科学中的种族包容性。

IF 14.7 1区医学

Neuron Pub Date : 2024-09-04 Epub Date: 2024-08-21 DOI: 10.1016/j.neuron.2024.08.004

Jose Rodriguez-Romaguera, Gregory J Quirk

引用次数: 0

Semaphorin 6D tunes amygdalar circuits for emotional, metabolic, and inflammatory outputs. Semaphorin 6D 可调节杏仁回路，促进情绪、新陈代谢和炎症输出。

IF 14.7 1区医学

Neuron Pub Date : 2024-09-04 Epub Date: 2024-07-12 DOI: 10.1016/j.neuron.2024.06.017

Yoshimitsu Nakanishi, Mayuko Izumi, Hiroaki Matsushita, Yoshihisa Koyama, Diego Diez, Hyota Takamatsu, Shohei Koyama, Masayuki Nishide, Maiko Naito, Yumiko Mizuno, Yuta Yamaguchi, Tomoki Mae, Yu Noda, Kamon Nakaya, Satoshi Nojima, Fuminori Sugihara, Daisuke Okuzaki, Masahito Ikawa, Shoichi Shimada, Sujin Kang, Atsushi Kumanogoh

{"title":"Semaphorin 6D tunes amygdalar circuits for emotional, metabolic, and inflammatory outputs.","authors":"Yoshimitsu Nakanishi, Mayuko Izumi, Hiroaki Matsushita, Yoshihisa Koyama, Diego Diez, Hyota Takamatsu, Shohei Koyama, Masayuki Nishide, Maiko Naito, Yumiko Mizuno, Yuta Yamaguchi, Tomoki Mae, Yu Noda, Kamon Nakaya, Satoshi Nojima, Fuminori Sugihara, Daisuke Okuzaki, Masahito Ikawa, Shoichi Shimada, Sujin Kang, Atsushi Kumanogoh","doi":"10.1016/j.neuron.2024.06.017","DOIUrl":"10.1016/j.neuron.2024.06.017","url":null,"abstract":"Regulated neural-metabolic-inflammatory responses are essential for maintaining physiological homeostasis. However, the molecular machinery that coordinates neural, metabolic, and inflammatory responses is largely unknown. Here, we show that semaphorin 6D (SEMA6D) coordinates anxiogenic, metabolic, and inflammatory outputs from the amygdala by maintaining synaptic homeostasis. Using genome-wide approaches, we identify SEMA6D as a pleiotropic gene for both psychiatric and metabolic traits in human. Sema6d deficiency increases anxiety in mice. When fed a high-fat diet, Sema6d-/- mice display attenuated obesity and enhanced myelopoiesis compared with control mice due to higher sympathetic activity via the β3-adrenergic receptor. Genetic manipulation and spatial and single-nucleus transcriptomics reveal that SEMA6D in amygdalar interneurons is responsible for regulating anxiogenic and autonomic responses. Mechanistically, SEMA6D is required for synaptic maturation and γ-aminobutyric acid transmission. These results demonstrate that SEMA6D is important for the normal functioning of the neural circuits in the amygdala, coupling emotional, metabolic, and inflammatory responses.","PeriodicalId":19313,"journal":{"name":"Neuron","volume":" ","pages":"2955-2972.e9"},"PeriodicalIF":14.7,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141603988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism. 小胶质细胞不是维持健康血脑屏障特性的必要条件，但 PLX5622 会改变脑内皮胆固醇代谢。

IF 14.7 1区医学

Neuron Pub Date : 2024-09-04 Epub Date: 2024-08-13 DOI: 10.1016/j.neuron.2024.07.015

Caterina P Profaci, Sean S Harvey, Kaja Bajc, Tony Z Zhang, Danielle A Jeffrey, Alexander Z Zhang, Kelsey M Nemec, Hayk Davtyan, Carleigh A O'Brien, Gabriel L McKinsey, Aaron Longworth, Timothy P McMullen, Joia K Capocchi, Jessica G Gonzalez, Devon A Lawson, Thomas D Arnold, Dimitrios Davalos, Mathew Blurton-Jones, Fabrice Dabertrand, F Chris Bennett, Richard Daneman

{"title":"Microglia are not necessary for maintenance of blood-brain barrier properties in health, but PLX5622 alters brain endothelial cholesterol metabolism.","authors":"Caterina P Profaci, Sean S Harvey, Kaja Bajc, Tony Z Zhang, Danielle A Jeffrey, Alexander Z Zhang, Kelsey M Nemec, Hayk Davtyan, Carleigh A O'Brien, Gabriel L McKinsey, Aaron Longworth, Timothy P McMullen, Joia K Capocchi, Jessica G Gonzalez, Devon A Lawson, Thomas D Arnold, Dimitrios Davalos, Mathew Blurton-Jones, Fabrice Dabertrand, F Chris Bennett, Richard Daneman","doi":"10.1016/j.neuron.2024.07.015","DOIUrl":"10.1016/j.neuron.2024.07.015","url":null,"abstract":"Microglia, the resident immune cells of the central nervous system, are intimately involved in the brain's most basic processes, from pruning neural synapses during development to preventing excessive neuronal activity throughout life. Studies have reported both helpful and harmful roles for microglia at the blood-brain barrier (BBB) in the context of disease. However, less is known about microglia-endothelial cell interactions in the healthy brain. To investigate the role of microglia at a healthy BBB, we used the colony-stimulating factor 1 receptor (CSF1R) inhibitor PLX5622 to deplete microglia and analyzed the BBB ultrastructure, permeability, and transcriptome. Interestingly, we found that, despite their direct contact with endothelial cells, microglia are not necessary for the maintenance of BBB structure, function, or gene expression in the healthy brain. However, we found that PLX5622 treatment alters brain endothelial cholesterol metabolism. This effect was independent from microglial depletion, suggesting that PLX5622 has off-target effects on brain vasculature.","PeriodicalId":19313,"journal":{"name":"Neuron","volume":" ","pages":"2910-2921.e7"},"PeriodicalIF":14.7,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11446403/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141982868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sequence variations and accessory proteins adapt TMC functions to distinct sensory modalities. 序列变异和附属蛋白使 TMC 功能适应不同的感觉模式。

IF 14.7 1区医学

Neuron Pub Date : 2024-09-04 Epub Date: 2024-07-09 DOI: 10.1016/j.neuron.2024.06.013

Qiang Jiang, Wenjuan Zou, Shitian Li, Xufeng Qiu, Linhui Zhu, Lijun Kang, Ulrich Müller

{"title":"Sequence variations and accessory proteins adapt TMC functions to distinct sensory modalities.","authors":"Qiang Jiang, Wenjuan Zou, Shitian Li, Xufeng Qiu, Linhui Zhu, Lijun Kang, Ulrich Müller","doi":"10.1016/j.neuron.2024.06.013","DOIUrl":"10.1016/j.neuron.2024.06.013","url":null,"abstract":"Transmembrane channel-like (TMC) proteins are expressed throughout the animal kingdom and are thought to encode components of ion channels. Mammals express eight TMCs (mTMC1-8), two of which (mTMC1 and mTMC2) are subunits of mechanotransduction channels. C. elegans expresses two TMCs (TMC-1 and TMC-2), which mediate mechanosensation, egg laying, and alkaline sensing. The mechanisms by which nematode TMCs contribute to such diverse physiological processes and their functional relationship to mammalian mTMCs is unclear. Here, we show that association with accessory proteins tunes nematode TMC-1 to divergent sensory functions. In addition, distinct TMC-1 domains enable touch and alkaline sensing. Strikingly, these domains are segregated in mammals between mTMC1 and mTMC3. Consistent with these findings, mammalian mTMC1 can mediate mechanosensation in nematodes, while mTMC3 can mediate alkaline sensation. We conclude that sequence diversification and association with accessory proteins has led to the emergence of TMC protein complexes with diverse properties and physiological functions.","PeriodicalId":19313,"journal":{"name":"Neuron","volume":" ","pages":"2922-2937.e8"},"PeriodicalIF":14.7,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11377162/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141580444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Impacts beyond the brain: Unraveling molecular mechanisms linking psychiatric, metabolic, and inflammatory conditions. 大脑之外的影响：揭示连接精神疾病、新陈代谢和炎症的分子机制。

IF 14.7 1区医学

Neuron Pub Date : 2024-09-04 DOI: 10.1016/j.neuron.2024.08.001

Nathaniel Napoli, Quenten Schwarz

引用次数: 0

Keep calm and carry H3K27me1 off. 保持冷静，将 H3K27me1 起飞。

IF 14.7 1区医学

Neuron Pub Date : 2024-09-04 DOI: 10.1016/j.neuron.2024.07.014

Rafael Alcalá-Vida, Angel Barco

引用次数: 0

Principles of cortical areas and their implications for neuroimaging. 皮层区域原理及其对神经影像学的影响。

IF 14.7 1区医学

Neuron Pub Date : 2024-09-04 Epub Date: 2024-06-03 DOI: 10.1016/j.neuron.2024.05.008

Steven E Petersen, Benjamin A Seitzman, Steven M Nelson, Gagan S Wig, Evan M Gordon

引用次数: 0

Sensory choices as logistic classification. 作为逻辑分类的感官选择

IF 14.7 1区医学

Neuron Pub Date : 2024-09-04 Epub Date: 2024-07-15 DOI: 10.1016/j.neuron.2024.06.016

Matteo Carandini

引用次数: 0

Mono-methylation of lysine 27 at histone 3 confers lifelong susceptibility to stress. 组蛋白 3 中赖氨酸 27 的单甲基化导致终生易受压力影响。

IF 14.7 1区医学

Neuron Pub Date : 2024-09-04 Epub Date: 2024-07-02 DOI: 10.1016/j.neuron.2024.06.006

Angélica Torres-Berrío, Molly Estill, Vishwendra Patel, Aarthi Ramakrishnan, Hope Kronman, Angélica Minier-Toribio, Orna Issler, Caleb J Browne, Eric M Parise, Yentl Y van der Zee, Deena M Walker, Freddyson J Martínez-Rivera, Casey K Lardner, Romain Durand-de Cuttoli, Scott J Russo, Li Shen, Simone Sidoli, Eric J Nestler

{"title":"Mono-methylation of lysine 27 at histone 3 confers lifelong susceptibility to stress.","authors":"Angélica Torres-Berrío, Molly Estill, Vishwendra Patel, Aarthi Ramakrishnan, Hope Kronman, Angélica Minier-Toribio, Orna Issler, Caleb J Browne, Eric M Parise, Yentl Y van der Zee, Deena M Walker, Freddyson J Martínez-Rivera, Casey K Lardner, Romain Durand-de Cuttoli, Scott J Russo, Li Shen, Simone Sidoli, Eric J Nestler","doi":"10.1016/j.neuron.2024.06.006","DOIUrl":"10.1016/j.neuron.2024.06.006","url":null,"abstract":"Histone post-translational modifications are critical for mediating persistent alterations in gene expression. By combining unbiased proteomics profiling and genome-wide approaches, we uncovered a role for mono-methylation of lysine 27 at histone H3 (H3K27me1) in the enduring effects of stress. Specifically, mice susceptible to early life stress (ELS) or chronic social defeat stress (CSDS) displayed increased H3K27me1 enrichment in the nucleus accumbens (NAc), a key brain-reward region. Stress-induced H3K27me1 accumulation occurred at genes that control neuronal excitability and was mediated by the VEFS domain of SUZ12, a core subunit of the polycomb repressive complex-2, which controls H3K27 methylation patterns. Viral VEFS expression changed the transcriptional profile of the NAc, led to social, emotional, and cognitive abnormalities, and altered excitability and synaptic transmission of NAc D1-medium spiny neurons. Together, we describe a novel function of H3K27me1 in the brain and demonstrate its role as a \"chromatin scar\" that mediates lifelong stress susceptibility.","PeriodicalId":19313,"journal":{"name":"Neuron","volume":" ","pages":"2973-2989.e10"},"PeriodicalIF":14.7,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11377169/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141498613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neuron最新文献