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The estrous cycle modulates hippocampal spine dynamics, dendritic processing, and spatial coding

Neuron 2025年

作者： Wolcott, Nora S. Redman, William T. Karpinska, Marie Jacobs, Emily G. Goard, Michael J. Department of Molecular Cellular and Developmental Biology University of California Santa Barbara Santa Barbara 93106 CA United States Interdepartmental Graduate Program in Dynamical Neuroscience University of California Santa Barbara Santa Barbara 93106 CA United States Intelligent Systems Center Johns Hopkins University Applied Physics Laboratory Laurel 20723 MD United States Department of Computer Science University of California Santa Barbara Santa Barbara 93106 CA United States Department of Psychological & Brain Sciences University of California Santa Barbara Santa Barbara 93106 CA United States Ann S. Bowers Women's Brain Health Initiative University of California Santa Barbara Santa Barbara 93106 CA United States Neuroscience Research Institute University of California Santa Barbara Santa Barbara 93106 CA United States

Histological evidence suggests that the estrous cycle exerts a powerful influence on CA1 neurons in the mammalian hippocampus. Decades have passed since this landmark observation, yet how the estrous cycle shapes dendritic spine dynamics and hippocampal spatial coding in vivo remains a mystery. Here, we used a custom hippocampal microperiscope and two-photon calcium imaging to track CA1 pyramidal neurons in female mice across multiple cycles. Estrous cycle stage had a potent effect on spine dynamics, with spine density peaking during proestrus when estradiol levels are highest. These morphological changes coincided with greater somatodendritic coupling and increased infiltration of back-propagating action potentials into the apical dendrite. Finally, tracking CA1 response properties during navigation revealed greater place field stability during proestrus, evident at both the single-cell and population levels. These findings demonstrate that the estrous cycle drives large-scale structural and functional plasticity in hippocampal neurons essential for learning and memory. © 2025 The Author(s)

关键词： dendritic integration estradiol estrous cycle hippocampus multiphoton imaging neuroendocrine place cells spine morphology

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OpenMM 8: Molecular Dynamics Simulation with Machine Learning Potentials

arXiv

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arXiv 2023年

作者： Eastman, Peter Galvelis, Raimondas Peláez, Raúl P. Abreu, Charlles R.A. Farr, Stephen E. Gallicchio, Emilio Gorenko, Anton Henry, Michael M. Hu, Frank Huang, Jing Krämer, Andreas Michel, Julien Mitchell, Joshua A. Pande, Vijay S. Rodrigues, João P.G.L.M. Rodriguez-Guerra, Jaime Simmonett, Andrew C. Singh, Sukrit Swails, Jason Turner, Philip Wang, Yuanqing Zhang, Ivy Chodera, John D. De Fabritiis, Gianni Markland, Thomas E. Department of Chemistry Stanford University StanfordCA94305 United States Acellera Labs C Dr Trueta 183 Barcelona08005 Spain C Dr. Aiguader 88 Barcelona08003 Spain Chemical Engineering Department School of Chemistry Federal University of Rio de Janeiro Rio de Janeiro68542 Brazil Redesign Science Inc. 180 Varick St. New YorkNY10014 United States EaStCHEM School of Chemistry University of Edinburgh EH9 3FJ United Kingdom Department of Chemistry and Biochemistry Brooklyn College The City University of New York NY United States Ph.D. Program in Chemistry Ph.D. Program in Biochemistry The Graduate Center of the City University of New York New YorkNY United States Stream HPC Koningin Wilhelminaplein 1 - 40601 Amsterdam1062 HG Netherlands Computational and Systems Biology Program Sloan Kettering Institute Memorial Sloan Kettering Cancer Center New YorkNY10065 United States Key Laboratory of Structural Biology of Zhejiang Province School of Life Sciences Westlake University 18 Shilongshan Road Zhejiang Hangzhou310024 China Department of Mathematics and Computer Science Freie Universität Berlin Arnimallee 12 Berlin14195 Germany The Open Force Field Initiative Open Molecular Software Foundation DavisCA95616 United States Andreessen Horowitz 2865 Sand Hill Rd Menlo ParkCA94025 United States Department of Structural Biology Stanford University StanfordCA94305 United States Charité Universitätsmedizin Berlin In silico Toxicology and Structural Bioinformatics Virchowweg 6 Berlin10117 Germany Laboratory of Computational Biology National Heart Lung and Blood Institute National Institutes of Health BethesdaMD20892 United States Entos Inc. 9310 Athena Circle La Jolla CA92037 United States College of Engineering Virginia Polytechnic Institute State University BlacksburgVA24061 United States Simons Center for Computational Physical Chemistry Center for Data Science New York University 24 Waverly Place New YorkNY10004 United States T

Machine learning plays an important and growing role in molecular simulation. The newest version of the OpenMM molecular dynamics toolkit introduces new features to support the use of machine learning potentials. Arbitrary PyTorch models can be added to a simulation and used to compute forces and energy. A higher-level interface allows users to easily model their molecules of interest with general purpose, pretrained potential functions. A collection of optimized CUDA kernels and custom PyTorch operations greatly improves the speed of simulations. We demonstrate these features on simulations of cyclin-dependent kinase 8 (CDK8) and the green fluorescent protein (GFP) chromophore in water. Taken together, these features make it practical to use machine learning to improve the accuracy of simulations at only a modest increase in cost. Copyright © 2023, The Authors. All rights reserved.

关键词： Machine learning

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Preliminary investigation of the association between epigenetic aging acceleration and amyloid biomarkers in bipolar disorder

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The American Journal of Geriatric Psychiatry 2025年

作者： Gabriel R. Fries Steven De La Garza Ning O. Zhao Andres W. Bass Camila N.C. Lima Nobuhide Kobori Tatiana Barichello Gustavo Turecki Paul E. Schulz Breno C. Diniz Jair C. Soares Translational Psychiatry Program Faillace Department of Psychiatry and Behavioral Sciences McGovern Medical School The University of Texas Health Science Center at Houston 1941 East Rd Houston Texas USA Neuroscience Graduate Program The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences 6767 Bertner Ave Houston Texas USA Center of Excellence in Mood Disorders Faillace Department of Psychiatry and Behavioral Sciences McGovern Medical School The University of Texas Health Science Center at Houston 1941 East Rd Houston Texas USA Department of Neurobiology and Anatomy McGovern Medical School The University of Texas Health Science Center at Houston 1941 East Rd Houston Texas USA Douglas Mental Health University Institute Department of Psychiatry McGill University Montreal Quebec Canada Department of Neurology McGovern Medical School The University of Texas Health Science Center at Houston Houston TX 77030 USA Neurocognitive Disorders Center McGovern Medical School The University of Texas Health Science Center at Houston Neurosciences Houston Texas USA UConn Center on Aging & Department of Psychiatry UConn School of Medicine University of Connecticut Health Center USA

Objectives Bipolar disorder (BD) has been associated with an elevated risk of Alzheimer’s Disease (AD). We assessed AD biomarkers in BD and tested whether epigenetic aging (EA) acceleration is associated with changes in these markers. Design, Setting, Participants Cross-sectional study of n=58 living individuals with BD and n=20 age- and sex-matched control participants, as well as analyses of postmortem brain samples (Brodmann area 9/46) from n=46 individuals with BD. Measurements Amyloid beta (Aβ) 40 , Aβ 42 , and total Tau levels were measured in plasma from individuals with BD and controls, and Aβ 42 levels were measured in brains. EA and its acceleration (blood: GrimAge and DunedinPACE; brains: DNAmClock Cortical ) were estimated for all samples. Individuals with BD were split into quartiles with accelerated or slower EA if they were in the first or fourth quartiles for GrimAge acceleration (AgeAccelGrim), DunedinPACE, or DNAmClock Cortical acceleration (DNAmClock Cortical Accel). Results Individuals with BD showed a decrease in the Aβ 42/40 ratio (p=.048) compared to controls, and a significant decrease in the Aβ 42/40 ratio was also found in individuals with BD with high versus low AgeAccelGrim (p=.048). Brain Aβ 42 levels significantly correlated with DNAmClock Cortical Accel (r 2 =.270, p=.007), with those with high EA acceleration showing higher brain Aβ 42 after controlling for confounders (p=.008). Conclusions Our results provide preliminary evidence that accelerated EA is associated with markers of AD in individuals with BD, suggesting it as a potential target in efforts to prevent dementia and AD in BD.

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Correction to: Mild traumatic brain injury induces microvascular injury and accelerates Alzheimer-like pathogenesis in mice

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Acta neuropathologica communications 2024年第1期12卷 27页

作者： Yingxi Wu Haijian Wu Jianxiong Zeng Brock Pluimer Shirley Dong Xiaochun Xie Xinying Guo Tenghuan Ge Xinyan Liang Sudi Feng Youzhen Yan Jian-Fu Chen Naomi Sta Maria Qingyi Ma Fernando Gomez-Pinilla Zhen Zhao Center for Neurodegeneration and Regeneration Zilkha Neurogenetic Institute Room: 241 1501 San Pablo Street 90033 Los Angeles CA USA. Department of Physiology and Biophysics Keck School of Medicine University of Southern California 90033 Los Angeles CA USA. Department of Neurosurgery Second Affiliated Hospital School of Medicine Zhejiang University 310009 Hangzhou Zhejiang China. Neuroscience Graduate Program Keck School of Medicine University of Southern California 90033 Los Angeles CA USA. Center for Craniofacial Molecular Biology Herman Ostrow School of Dentistry University of Southern California 90033 Los Angeles CA USA. Lawrence D. Longo MD Center for Perinatal Biology Division of Pharmacology Department of Basic Sciences Loma Linda University School of Medicine 92350 Loma Linda CA USA. Brain Injury Research Center Department of Neurosurgery University of California Los Angeles 90095 Los Angeles CA USA. Center for Neurodegeneration and Regeneration Zilkha Neurogenetic Institute Room: 241 1501 San Pablo Street 90033 Los Angeles CA USA. zzhao@usc.edu. Department of Physiology and Biophysics Keck School of Medicine University of Southern California 90033 Los Angeles CA USA. zzhao@usc.edu. Neuroscience Graduate Program Keck School of Medicine University of Southern California 90033 Los Angeles CA USA. zzhao@usc.edu.

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Characterization of antipsychotic medications, amino acid signatures, and platelet-activating factor in first-episode psychosis

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Biomarkers in Neuropsychiatry 2021年 5卷 100045-100045页

作者： Avigdor, Bracha Erlanger Yang, Kun Shinder, Ida Orsburn, Benjamin C. Rais, Rana Kano, Shin-ichi Sawa, Akira Pevsner, Jonathan Department of Neurology Kennedy Krieger Institute United States Department of Psychiatry and Behavioral Sciences Johns Hopkins School of Medicine United States Cross Disciplinary Graduate Program in Biomedical Sciences Johns Hopkins School of Medicine United States Department of Pharmacology and Molecular Sciences Johns Hopkins School of Medicine United States Department of Neurology Johns Hopkins School of Medicine United States Department of Biomedical Engineering Johns Hopkins University School of Medicine United States Department of Neuroscience Johns Hopkins University School of Medicine United States Department of Mental Health Johns Hopkins University Bloomberg School of Public Health 600N. Wolfe Street Baltimore 21287 MD United States

First-episode psychosis refers to individuals early in the course of psychotic illness. Identifying the underlying biological processes, including biomarkers, is essential for improving diagnosis and treatment. We performed metabolomics profiling of plasma from a group of first-episode psychosis patients and matched neurotypical controls. Using global metabolomics profiling, we identified antipsychotic or antidepressant medication in 22 individuals diagnosed with first-episode psychosis, closely matching the drug prescription history. There were significant differences in levels of amino acids or their derivatives, including decreases in DL-arginine, L-histidine, DL-serine and threonine as well as increases in L-glutamic acid, ornithine, and proline. Using targeted metabolomics profiling of 408 compounds in plasma samples we identified significant differences in six compounds including decreases in serotonin and arginine as well as increased levels of sarcosine, proline, cis-4-hydroxyproline and trans-4-hydroxyproline. Platelet-activating factor levels were significantly elevated in the FEP cohort. These findings suggest potential biomarkers that require validation in independent cohorts, and in several cases provide supporting evidence for previously reported observations. © 2021

关键词： Antipsychotics Biomarkers Bipolar disorder Metabolites Metabolomics Schizophrenia

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Sensory experience remodels genome architecture in neural circuit to drive motor learning (vol 569, pg 708, 2019)

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NATURE 2019年第7760期570卷 E33-E33页

作者： Yamada, Tomoko Yang, Yue Valnegri, Pamela Juric, Ivan Abnousi, Armen Markwalter, Kelly H. Guthrie, Arden N. Godec, Abigail Oldenborg, Anna Hu, Ming Holy, Timothy E. Bonni, Azad Department of Neuroscience Washington University School of Medicine St. Louis USA Faculty of Medicine University of Tsukuba Tsukuba Japan Department of Neurobiology Northwestern University Evanston USA Department of Quantitative Health Sciences Lerner Research Institute Cleveland Clinic Foundation Cleveland USA MD-PhD Program Washington University School of Medicine St. Louis USA

In this Letter, '≥' should be '≤' in the sentence: "Intra-chromosomal reads were further split into short-range reads (≥1 kb) and long-range reads (>1 kb)". This error has been correcte...

In this Letter, '≥' should be '≤' in the sentence: "Intra-chromosomal reads were further split into short-range reads (≥1 kb) and long-range reads (>1 kb)". This error has been corrected *** amendment to this paper has been published and can be accessed via a link at the top of the paper.

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Correction to: Genomic Action of Sigma-1 Receptor Chaperone Relates to Neuropathic Pain

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Molecular neurobiology 2021年第6期58卷 2542页

作者： Shao-Ming Wang Nino Goguadze Yuriko Kimura Yuko Yasui Bin Pan Tzu-Yun Wang Yoki Nakamura Yu-Ting Lin Quinn H Hogan Katherine L Wilson Tsung-Ping Su Hsiang-En Wu Cellular Pathobiology Section Integrative Neuroscience Research Branch Intramural Research Program National Institute on Drug Abuse NIH/DHHS Suite 3512 333 Cassell Drive Baltimore MD 21224 USA. Department of Anesthesiology Medical College of Wisconsin Milwaukee WI 53226 USA. Department of Psychiatry College of Medicine National Cheng Kung University Tainan City 70101 Taiwan. Department of Pharmacology Graduate School of Biomedical & Health Science Hiroshima University Hiroshima 734-8553 Japan. Department of Cell Biology Johns Hopkins University School of Medicine Baltimore MD 21205 USA. Cellular Pathobiology Section Integrative Neuroscience Research Branch Intramural Research Program National Institute on Drug Abuse NIH/DHHS Suite 3512 333 Cassell Drive Baltimore MD 21224 USA. TSU@intra.nida.nih.gov.

A correction to this paper has been published: 10.1007/s12035-021-02310-3

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Anterior cingulate and Hippocampus neurometabolites profile in Bipolar Disorder: an ENIGMA Bipolar meta-analysis

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neuroscience Applied 2024年 3卷

作者： E. Scotti-Muzzi B. Sottili B. Haarman F. Howells D. Stein F. Scheffler F. Benedetti M. Green Y. Quide M. Berk J. Prisciandaro J. Soares M.J. Wu B. Mwangi J. Stone L. Jelen D. Hermens T. Hajek L. Yatham M. Kang M. Otaduy State University of Rio de Janeiro UERJ Department of Psychiatry- Pedro Ernesto University Hospital Rio De Janeiro Brazil University of São Paulo Institute of Psychiatry São Paulo Brazil University Medical Center Gronningen University of Groningen Groningen Netherlands University of Cape Town Department of Psychiatry and Mental Health Cape Town South Africa San Raffaele Scientific Institute Department of Clinical Neuroscience Millano Italy UNSW Sydney Imaging Genetics in Psychosis IGP Sydney Australia UNSW Sydney School of Psychology Sydney Australia Deakin University Institute for Mental and Physical Health and Clinical Translation Victoria Australia Medical University of South Carolina Department of Psychiatry and Behavioral Sciences Charleston United States The University of Texas Health Science Center at Houston Louis A. Faillace- MD- Department of Psychiatry and Behavioral Sciences- McGovern Medical School Houston United States University of Sussex Trafford Centre for Medical Research Brighton United Kingdom King's College London Department of Psychological Medicine London United Kingdom University of the Sunshine Coast USC · Sunshine Coast Mind and Neuroscience – Thompson Institute Sippy Downs Australia Dalhousie University Department of Psychiatry Halifax Canada University of British Columbia Department of Psychiatry Vancouver Canada University of Southern California Neuroscience Graduate Program Los Angeles United States University of São Paulo Institute of Radiology São Paulo Brazil

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Correction : IL-1R1 signaling in TBI: assessing chronic impacts and neuroinflammatory dynamics in a mouse model of mild closed-head injury

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Journal of neuroinflammation 2023年第1期20卷 287页

作者： Jonathan C Vincent Colleen N Garnett James B Watson Emma K Higgins Teresa Macheda Lydia Sanders Kelly N Roberts Ryan K Shahidehpour Eric M Blalock Ning Quan Adam D Bachstetter Department of Neuroscience University of Kentucky 741 S. Limestone St. Lexington KY 40536 USA. Spinal Cord and Brain Injury Research Center University of Kentucky Lexington KY USA. Sanders‑Brown Center on Aging University of Kentucky Lexington KY USA. MD/PhD Program University of Kentucky Lexington KY USA. Department of Cell Developmental and Integrative Biology University of Alabama at Birmingham Birmingham AL USA. Department of Pharmacology and Nutritional Sciences University of Kentucky Lexington KY USA. Department of Biomedical Science Charles E. Schmidt College of Medicine and Brain Institute Florida Atlantic University Jupiter FL USA. Department of Neuroscience University of Kentucky 741 S. Limestone St. Lexington KY 40536 USA. adam.bachstetter@uky.edu. Spinal Cord and Brain Injury Research Center University of Kentucky Lexington KY USA. adam.bachstetter@uky.edu. Sanders‑Brown Center on Aging University of Kentucky Lexington KY USA. adam.bachstetter@uky.edu.

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Optogenetic activation of cortical microglia promotes neuronal activity and pain hypersensitivity

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Cell Reports 2025年第5期44卷 115717页

作者： Yi, Min-Hee Liu, Yi Liu, Yong U. Lee, Jinkyung Hanumaihgari, Priyanka Parusel, Sebastian Bosco, Dale B. Wang, Lingxiao Zheng, Jiaying Shi, Wu Eauchai, Lattawat Chompoopong, Supin Hunt, Christine L. Wu, Long-Jun Department of Neurology Mayo Clinic Rochester 55905 MN United States Department of Microbiology and Immunology Chonnam National University Medical School Jeollanam-do Hwasun 58128 South Korea Institute for Biomedical Science (IBS) of Chonnam National University Hwasun Hospital Jeollanam-do Hwasun 58128 South Korea BioMedical Sciences Graduate Program (BMSGP) Chonnam National University Jeollanam-do Hwasun 58128 South Korea Center for Neuroimmunology and Glial Biology Institute of Molecular Medicine University of Texas Health Science Center Houston 77030 TX United States Department of Anesthesiology First Affiliated Hospital of Sun Yat-sen University Guangdong Guangzhou 510080 China Department of Anesthesiology Guangzhou First People's Hospital School of Medicine South China University of Technology Guangzhou China Department of Neuroscience Johns Hopkins Medical Institute Baltimore 21205 MD United States Faculty of Medicine Siriraj Hospital Mahidol University Bangkok 10700 Thailand Department of Pain Medicine Mayo Clinic Jacksonville 32224 FL United States

Chronic pain following peripheral nerve injury is accompanied by increased neuronal activity in the somatosensory cortex. However, whether and how cortical microglia contribute to these changes is less understood. To this end, we applied an optogenetic strategy to specifically target cortical microglia and investigate their function in behavioral pain sensitization. We found that optogenetic activation of microglia in the primary somatosensory cortex (S1) via red-activated channelrhodopsin (ReaChR) triggered pain hypersensitivity and affective-motivational responses in mice. Remarkably, S1-targeted optogenetic stimulation increased microglial landscape changes and ATP release. In addition, optogenetic stimulation altered the microglial proteomic profile, upregulated neuronal c-Fos expression, and enhanced neuronal Ca²⁺ signaling in the S1. Our results provide mechanistic evidence linking cortical microglia with neuronal hyperactivity and chronic pain behaviors. © 2025 The Author(s)

关键词： ATP chronic pain CP: neuroscience microglia microglial landscape change optogenetics ReaChR somatosensory cortex two-photon imaging

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