研究活動情報

• 2024年 神戸大学医学部, 神戸大学医学部優秀学術論文賞


• 2024年 敬愛まちづくり財団, 前之園記念若手優秀論文賞


• 2019年02月 平成30年度文部科学省新学術領域研究 学術研究支援基盤形成 先端モデル動物支援プラットフォーム, 優秀ポスター賞

  中井信裕


• 2017年 日本神経科学学会, JNS-SfN Exchange Travel Award

  中井信裕

• Subtype-specific modulation of inhibitory interneurons by general anesthetics

  Taisuke Sugino, Takuya Okada, Yuki Nomura, Riko Nakayama, Midori Harada, Nobuhiro Nakai, Norihiko Obata, Satoshi Mizobuchi

  Elsevier BV, 2026年03月, iScience, 29(3) (3), 115140 - 115140

  [査読有り]

  研究論文（学術雑誌）


• Parvalbumin interneurons in the insular cortex control social familiarity and emotion recognition.

  Shuhei Fujima, Masaaki Sato, Nobuhiro Nakai, Toru Takumi

  The insular cortex is involved in various aspects of social behavior, yet the role and mechanism of its inhibitory regulation remain unclear. Through cell-type-specific microendoscopic calcium imaging and chemogenetic manipulation of neuronal activity, we discovered that parvalbumin-positive interneurons (PVINs) in the agranular insular cortex (aIC) are crucial in governing social familiarity and emotion recognition. Like pyramidal neurons (PNs), a specific subset of PVINs showed increased activity during peer interactions. Inhibiting PVINs led to a failure in losing the preference for familiar peers and hindered the rise in interactions with stressed individuals. These changes in behavior were linked to alterations in the proportion of PNs that showed activity corresponding to interactions with significant peers and the transitions in their social target specificity across sessions. Our findings highlight that PVINs provide context-dependent control over socioemotional behavior and the coding of social information by locally adjusting the social preference of individual PNs in the aIC.

  2025年09月, Cell reports, 44(9) (9), 116085 - 116085, 英語, 国際誌

  [査読有り]

  研究論文（学術雑誌）

  神戸大学リポジトリ（Kernel）へのリンク


• ESC models of autism with copy-number variations reveal cell-type-specific translational vulnerability.

  Jun Nomura, Amila Zuko, Keiko Kishimoto, Hiroaki Mutsumine, Hiroko Maegawa, Kazumi Fukatsu, Yoshiko Nomura, Xiaoxi Liu, Nobuhiro Nakai, Eiki Takahashi, Tsukasa Kouno, Jay W Shin, Toru Takumi

  Human genetics has identified numerous copy-number variations (CNVs) associated with autism spectrum disorders (ASDs). However, the lack of standardized biological resources impedes understanding of the cell-type-specific common features of ASD. Here, we establish a biological resource including 63 genetically modified mouse embryonic stem cell (ESC) lines as genetic models of ASD. We perform neural differentiation using 12 representative cell lines, and their comprehensive analyses, including single-cell RNA sequencing, uncover cell-type-specific susceptible pathways. Moreover, we find that a common phenotype in glutamatergic and GABAergic neurons is reduced expression of Upf3b, a core member of the translational termination and nonsense-mediated decay (NMD). This finding emphasizes that the dysfunction of translational machinery in the developing neurons can be a possible target of early intervention for ASD. This ESC model bank becomes an invaluable resource for studies in vitro and in vivo of ASD or other neuropsychiatric disorders.

  2025年06月, Cell genomics, 5(6) (6), 100877 - 100877, 英語, 国際誌

  [査読有り]

  研究論文（学術雑誌）

  神戸大学リポジトリ（Kernel）へのリンク


• Assigning Targetable Molecular Pathways to Transdiagnostic Subgroups Across Autism and Related Neurodevelopmental Disorders

  Jacob Ellegood, Antoine Beauchamp, Yohan Yee, Gabe Devenyi, Justine Ziolkowski, Lily Qiu, Rand Askalan, Muhammad Ayub, Philipp Suetterlin, Alex Donovan, M. Albert Basson, Katherine M Quesnel, Nathalie G Berube, Taeseon Woo, David Beversdorf, Hans Bjornsson, Randy Blakely, Jacqueline Crawley, Jennifer Crosbie, Brian O Orr, Graeme W Davis, Matthew Genestine, Emanuel DiCicco-Bloom, Sean Egan, Kyle D Fink, Sarah Asbury, Jonathan Lai, Kelly Rilett, Jane A Foster, John B Vincent, Paul Frankland, Stelios Georgiades, Olga Penagarikano, Daniel Geschwind, Roman J Giger, Sander Markx, Joseph Gogos, Christelle Golzio, Marco Pagani, Alessandro Gozzi, Laura K Pacey, David Hampson, Tzyy-Nan Huang, Tzu-Li Yen, Yi-Ping Hsueh, Alana Iaboni, Megha Amar, Lilia M Iakoucheva, Jessica K Jones, Elizabeth Kelly, Brigette Kieffer, Mihyun Bae, Hwajin Jung, Hyosang Kim, Haram Park, Junye Daniel Roh, Eunjoon Kim, Genevieve Konopka, Christine Laliberte, Julie L Lefebvre, Kathie Eagleson, Pat Levitt, Aurea Martins Bach, Thomas J Cunningham, Elizabeth Fisher, Karla Miller, Alea Mills, Alyson Muotri, Rob Nicolson, Leigh Spencer Noakes, Brian J Nieman, Cesar P Canales, Alex S Nord, Lauryl MJ Nutter, Elaine Tam, Lucy R. Osborne, Amy Clipperton-Allen, Damon Page, Brooke Babineau, Theo D Palmer, Keqin Yan, David Picketts, Qiangqiang Xia, Craig M Powell, Armin Raznahan, Diane M Robins, Gavin Rumbaugh, Ameet S Sengar, Michael William SALTER, Russell James Schachar, Lia D'Abate, Clarissa A Bradley, Stephen W. Scherer, Nycole W. Copping, Stela P Petkova, Jill L Silverman, Karun Kar Singh, Nam-Shik Kim, Ki-Jun Kar Yoon, Guo-Li Ming, Hongjun Song, Shoshana Spring, Jin Nakatani, Nobuhiro Nakai, J Nomura, Toru Takumi, Margot Taylor, Peter Tsai, Matthew Bruce, Karen L Jones, Judy Van de Water, Matthijs C Van Eede, Travis M Kerr, Christopher L Muller, Jeremy Veenstra VanderWeele, Marlee Vandewouw, Rosanna Weksberg, Rachel Wevrick, Haim Belinson, Anthony Wynshaw-Boris, Konstantinos Zarbalis, Brett Trost, Rogier B Mars, Mallar Chakravarty, Azadek Kushki, Evdokia Anagnostou, Jason P Lerch

  Significant genetic, behavioural and neuroanatomic heterogeneity is common in autism spectrum- and related- neurodevelopmental disorders (NDDs). This heterogeneity constrains the development of effective therapies for diverse patients in precision medicine paradigms. This has led to the search for subgroups of individuals having common etiologic factors/biology (e.g., genetic pathways), thus creating potential uniformity in prognosis and/or treatment response. Despite NDDs having a strong genetic component, only ~15-20% of individuals will present with a specific rare genetic variant considered clinically pathogenic, and therefore, subtyping efforts tend to focus on using clinical, cognitive, and/or brain imaging phenotypes to group individuals. Here we delineated mechanisms via mouse to human translational neuroscience. Using MRI derived structural neuroanatomy and a spatial transcriptomic comparison, we linked subgroups of 135 NDD relevant mouse models (3,515 individual mice) separately to two human databases, with 1,234 and 1,015 human individuals with NDDs, composed of autism, attention-deficit/hyperactivity disorder (ADHD), obsessive compulsive disorder (OCD), other related NDDs, and typically developing controls. Subgroups were significantly linked by consistent neuroanatomy across all three datasets, mouse and human, indicating that direct cross-species subgrouping and translation is consistent and reproducible. Ultimately, four specific neuroanatomical clusters were found and linked to precise molecular mechanisms: two showing a chromatin/transcription motif, with one of those showing specific links to G-protein coupled receptors (GPCR) and Notch signalling, and another two being mainly synaptic in origin, with one off those showing specific connections to axon guidance and Wnt signaling. Assigning molecular pathways, and thus genetic information, from the mouse to individual participants provides an insight into undetected and/or related genetic variants that could be working in combination or interacting with an environmental influence. Moreover, the subgroups found are transdiagnostic, including participants with autism, ADHD, and OCD, which indicates that NDDs as a whole can be subdivided into consistent neuroanatomical clusters with cohesive underlying biological mechanisms. This work allows us to bridge the gap between preclinical models and human disorders, linking previously idiopathic human patients to pertinent genetics, molecular mechanisms, and pathways.

  Cold Spring Harbor Laboratory, 2025年03月


• End-to-end deep learning approach to mouse behavior classification from cortex-wide calcium imaging.

  Takehiro Ajioka, Nobuhiro Nakai, Okito Yamashita, Toru Takumi

  Deep learning is a powerful tool for neural decoding, broadly applied to systems neuroscience and clinical studies. Interpretable and transparent models that can explain neural decoding for intended behaviors are crucial to identifying essential features of deep learning decoders in brain activity. In this study, we examine the performance of deep learning to classify mouse behavioral states from mesoscopic cortex-wide calcium imaging data. Our convolutional neural network (CNN)-based end-to-end decoder combined with recurrent neural network (RNN) classifies the behavioral states with high accuracy and robustness to individual differences on temporal scales of sub-seconds. Using the CNN-RNN decoder, we identify that the forelimb and hindlimb areas in the somatosensory cortex significantly contribute to behavioral classification. Our findings imply that the end-to-end approach has the potential to be an interpretable deep learning method with unbiased visualization of critical brain regions.

  2024年03月, PLoS computational biology, 20(3) (3), e1011074, 英語, 国際誌

  [査読有り]

  研究論文（学術雑誌）

  神戸大学リポジトリ（Kernel）へのリンク


• Social circuits and their dysfunction in autism spectrum disorder.

  Masaaki Sato, Nobuhiro Nakai, Shuhei Fujima, Katrina Y Choe, Toru Takumi

  Social behaviors, how individuals act cooperatively and competitively with conspecifics, are widely seen across species. Rodents display various social behaviors, and many different behavioral paradigms have been used for investigating their neural circuit bases. Social behavior is highly vulnerable to brain network dysfunction caused by neurological and neuropsychiatric conditions such as autism spectrum disorders (ASDs). Studying mouse models of ASD provides a promising avenue toward elucidating mechanisms of abnormal social behavior and potential therapeutic targets for treatment. In this review, we outline recent progress and key findings on neural circuit mechanisms underlying social behavior, with particular emphasis on rodent studies that monitor and manipulate the activity of specific circuits using modern systems neuroscience approaches. Social behavior is mediated by a distributed brain-wide network among major cortical (e.g., medial prefrontal cortex (mPFC), anterior cingulate cortex, and insular cortex (IC)) and subcortical (e.g., nucleus accumbens, basolateral amygdala (BLA), and ventral tegmental area) structures, influenced by multiple neuromodulatory systems (e.g., oxytocin, dopamine, and serotonin). We particularly draw special attention to IC as a unique cortical area that mediates multisensory integration, encoding of ongoing social interaction, social decision-making, emotion, and empathy. Additionally, a synthesis of studies investigating ASD mouse models demonstrates that dysfunctions in mPFC-BLA circuitry and neuromodulation are prominent. Pharmacological rescues by local or systemic (e.g., oral) administration of various drugs have provided valuable clues for developing new therapeutic agents for ASD. Future efforts and technological advances will push forward the next frontiers in this field, such as the elucidation of brain-wide network activity and inter-brain neural dynamics during real and virtual social interactions, and the establishment of circuit-based therapy for disorders affecting social functions.

  2023年08月, Molecular psychiatry, 英語, 国際誌

  [査読有り]

  研究論文（学術雑誌）

  神戸大学リポジトリ（Kernel）へのリンク


• Virtual reality-based real-time imaging reveals abnormal cortical dynamics during behavioral transitions in a mouse model of autism.

  Nobuhiro Nakai, Masaaki Sato, Okito Yamashita, Yukiko Sekine, Xiaochen Fu, Junichi Nakai, Andrew Zalesky, Toru Takumi

  Functional connectivity (FC) can provide insight into cortical circuit dysfunction in neuropsychiatric disorders. However, dynamic changes in FC related to locomotion with sensory feedback remain to be elucidated. To investigate FC dynamics in locomoting mice, we develop mesoscopic Ca2+ imaging with a virtual reality (VR) environment. We find rapid reorganization of cortical FC in response to changing behavioral states. By using machine learning classification, behavioral states are accurately decoded. We then use our VR-based imaging system to study cortical FC in a mouse model of autism and find that locomotion states are associated with altered FC dynamics. Furthermore, we identify FC patterns involving the motor area as the most distinguishing features of the autism mice from wild-type mice during behavioral transitions, which might correlate with motor clumsiness in individuals with autism. Our VR-based real-time imaging system provides crucial information to understand FC dynamics linked to behavioral abnormality of neuropsychiatric disorders.

  2023年03月, Cell reports, 112258 - 112258, 英語, 国際誌

  [査読有り]

  研究論文（学術雑誌）

  神戸大学リポジトリ（Kernel）へのリンク


• Genetic dissection identifies Necdin as a driver gene in a mouse model of paternal 15q duplications.

  Kota Tamada, Keita Fukumoto, Tsuyoshi Toya, Nobuhiro Nakai, Janak R Awasthi, Shinji Tanaka, Shigeo Okabe, François Spitz, Fumihito Saitow, Hidenori Suzuki, Toru Takumi

  Maternally inherited duplication of chromosome 15q11-q13 (Dup15q) is a pathogenic copy number variation (CNV) associated with autism spectrum disorder (ASD). Recently, paternally derived duplication has also been shown to contribute to the development of ASD. The molecular mechanism underlying paternal Dup15q remains unclear. Here, we conduct genetic and overexpression-based screening and identify Necdin (Ndn) as a driver gene for paternal Dup15q resulting in the development of ASD-like phenotypes in mice. An excess amount of Ndn results in enhanced spine formation and density as well as hyperexcitability of cortical pyramidal neurons. We generate 15q dupΔNdn mice with a normalized copy number of Ndn by excising its one copy from Dup15q mice using a CRISPR-Cas9 system. 15q dupΔNdn mice do not show ASD-like phenotypes and show dendritic spine dynamics and cortical excitatory-inhibitory balance similar to wild type animals. Our study provides an insight into the role of Ndn in paternal 15q duplication and a mouse model of paternal Dup15q syndrome.

  2021年07月, Nature communications, 12(1) (1), 4056 - 4056, 英語, 国際誌

  [査読有り]

  研究論文（学術雑誌）

  神戸大学リポジトリ（Kernel）へのリンク


• Optogenetic Approaches to Understand the Neural Circuit Mechanism of Social Deficits Seen in Autism Spectrum Disorders.

  Nobuhiro Nakai, Eric T N Overton, Toru Takumi

  Individuals with neurodevelopmental disorders, such as autism spectrum disorders (ASDs), are diagnosed based on nonquantitative objective parameters such as behavioral phenotypes. It is still unclear how any neural mechanism affects such behavioral phenotypes in these patients. In human genetics, a large number of genetic abnormalities including single nucleotide variation (SNV) and copy number variation (CNV) have been found in individuals with ASDs. It is thought that influence of such variations converges on dysfunction of neural circuit resulting in common behavioral phenotypes of ASDs such as deficits in social communication and interaction. Recent studies suggest that an excitatory/inhibitory (E/I) imbalanced state, which induces disruption of neural circuit activities, is one of the pathophysiological abnormalities in ASD brains. To assess the causal relationship between brain abnormalities and behavioral deficits, we can take advantage of optogenetics with animal models of ASDs that recapitulate human genetic mutations. Here, we review optogenetics studies being utilized to dissect neural circuit mechanisms associated with social deficits in model mice of ASD. Optogenetic manipulation of disrupted neural activities would help us understand how neural circuits affect behavioral deficits observed in ASDs.

  2021年, Advances in experimental medicine and biology, 1293, 523 - 533, 英語, 国際誌

  研究論文（学術雑誌）


• Encoding of social exploration by neural ensembles in the insular cortex

  Isamu Miura, Masaaki Sato, Eric T. N. Overton, Nobuo Kunori, Junichi Nakai, Takakazu Kawamata, Nobuhiro Nakai, Toru Takumi

  The insular cortex (IC) participates in diverse complex brain functions, including social function, yet their cellular bases remain to be fully understood. Using microendoscopic calcium imaging of the agranular insular cortex (AI) in mice interacting with freely moving and restrained social targets, we identified 2 subsets of AI neurons-a larger fraction of "Social-ON" cells and a smaller fraction of "Social-OFF" cells-that change their activity in opposite directions during social exploration. Social-ON cells included those that represented social investigation independent of location and consisted of multiple subsets, each of which was preferentially active during exploration under a particular behavioral state or with a particular target of physical contact. These results uncover a previously unknown function of AI neurons that may act to monitor the ongoing status of social exploration while an animal interacts with unfamiliar conspecifics.

  Public Library of Science (PLoS), 2020年09月, PLOS Biology, 18(9) (9), e3000584 - e3000584, 英語, 国際誌

  [査読有り]

  研究論文（学術雑誌）

  神戸大学リポジトリ（Kernel）へのリンク


• Imaging the Neural Circuit Basis of Social Behavior: Insights from Mouse and Human Studies.

  Isamu Miura, Eric T N Overton, Nobuhiro Nakai, Takakazu Kawamata, Masaaki Sato, Toru Takumi

  Social behavior includes a variety of behaviors that are expressed between two or more individuals. In humans, impairment of social function (i.e., social behavior and social cognition) is seen in neurodevelopmental and neurological disorders including autism spectrum disorders (ASDs) and stroke, respectively. In basic neuroscience research, fluorescence monitoring of neural activity, such as immediate early gene (IEG)-mediated whole-brain mapping, fiber photometry, and calcium imaging using a miniaturized head-mounted microscope or a two-photon microscope, and non-fluorescence imaging such as functional magnetic resonance imaging (fMRI) are increasingly used to measure the activity of many neurons and multiple brain areas in animals during social behavior. In this review, we overview recent rodent studies that have investigated the dynamics of brain activity during social behavior at the whole-brain and local circuit levels and studies that explored the neural basis of social function in healthy, in brain-injured, and in autistic human subjects. A synthesis of such findings will advance our understanding of brain mechanisms underlying social behavior and facilitate the development of pharmaceutical and functional neurosurgical interventions for brain disorders affecting social function.

  2020年09月, Neurologia medico-chirurgica, 60(9) (9), 429 - 438, 英語, 国内誌

  [査読有り]

  研究論文（学術雑誌）


• Imaging the neural circuit basis of social behavior: insights from mouse and human studies

  Miura I, Overton ETN, Nakai N, Kawamata T, Sato M, Takumi T

  2020年06月, Neurol. Med. Chir (Tokyo), in press

  [査読有り]


• Altered microbiota composition reflects enhanced communication in 15q11-13 CNV mice.

  Dian Eurike Septyaningtrias, Chia-Wen Lin, Rika Ouchida, Nobuhiro Nakai, Wataru Suda, Masahira Hattori, Hidetoshi Morita, Kenya Honda, Kota Tamada, Toru Takumi

  Autism spectrum disorder (ASD) is a complex and heterogeneous neurodevelopmental disorder. In addition to the core symptoms of ASD, many patients with ASD also show comorbid gut dysbiosis, which may lead to various gastrointestinal (GI) problems. Intriguingly, there is evidence that gut microbiota communicate with the central nervous system to modulate behavioral output through the gut-brain axis. To investigate how the microbiota composition is changed in ASD and to identify which microbes are involved in autistic behaviors, we performed a 16S rRNA gene-based metagenomics analysis in an ASD mouse model. Here, we focused on a model with human 15q11-13 duplication (15q dup), the most frequent chromosomal aberration or copy number variation found in ASD. Species diversity of the microbiome was significantly decreased in 15q dup mice. A combination of antibiotics treatment and behavioral analysis showed that neomycin improved social communication in 15q dup mice. Furthermore, comparison of the microbiota composition of mice treated with different antibiotics enabled us to identify beneficial operational taxonomic units (OTUs) for ultrasonic vocalization.

  2019年12月, Neuroscience research, 161, 59 - 67, 英語, 国際誌

  [査読有り]

  研究論文（学術雑誌）


• Behavioral neuroscience of autism.

  Takumi T, Tamada K, Hatanaka F, Nakai N, Bolton PF

  Autism spectrum disorder (ASD) is a neurodevelopmental disorder. Several genetic causes of ASD have been identified and this has enabled researchers to construct mouse models. Mouse behavioral tests reveal impaired social interaction and communication, as well as increased repetitive behavior and behavioral inflexibility in these mice, which correspond to core behavioral deficits observed in individuals with ASD. However, the connection between these behavioral abnormalities and the underlying dysregulation in neuronal circuits and synaptic function is poorly understood. Moreover, different components of the ASD phenotype may be linked to dysfunction in different brain regions, making it even more challenging to chart the pathophysiological mechanisms involved in ASD. Here we summarize the research on mouse models of ASD and their contribution to understanding pathophysiological mechanisms. Specifically, we emphasize abnormal serotonin production and regulation, as well as the disruption in circadian rhythms and sleep that are observed in a subset of ASD, and propose that spatiotemporal disturbances in brainstem development may be a primary cause of ASD that propagates towards the cerebral cortex.

  2019年05月, Neuroscience and biobehavioral reviews, 110, 60 - 76, 英語, 国際誌

  [査読有り]

  研究論文（学術雑誌）


• 自閉症の分子メカニズム

  中井 信裕, 内匠 透

  (公社)日本生化学会, 2018年08月, 生化学, 90(4) (4), 462 - 477, 日本語

  [査読有り]


• Common defects of spine dynamics and circuit function in neurodevelopmental disorders: A systematic review of findings from in vivo optical imaging of mouse models

  Nobuhiro Nakai, Toru Takumi, Junichi Nakai, Masaaki Sato

  Frontiers Media S.A., 2018年06月, Frontiers in Neuroscience, 12, 412, 英語

  [査読有り]


• 脳神経回路と精神生物学 神経機能と心の根源を探る Caイメージングと精神神経機能

  三浦 勇, 中井 信裕, 戸谷 豪志, 川俣 貴一, 内匠 透

  (株)医薬ジャーナル社, 2018年04月, Clinical Calcium, 28(5) (5), 702 - 708, 日本語


• 自閉症研究の最前線 基礎から臨床までの多面的なアプローチ 自閉症のモデル研究

  内匠 透, 中井 信裕

  東北医学会, 2017年06月, 東北医学雑誌, 129(1) (1), 26 - 27, 日本語


• Serotonin rebalances cortical tuning and behavior linked to autism symptoms in 15q11-13 CNV mice

  Nobuhiro Nakai, Masatoshi Nagano, Fumihito Saitow, Yasuhito Watanabe, Yoshinobu Kawamura, Akiko Kawamoto, Kota Tamada, Hiroshi Mizuma, Hirotaka Onoe, Yasuyoshi Watanabe, Hiromu Monai, Hajime Hirase, Jin Nakatani, Hirofumi Inagaki, Tomoyuki Kawada, Taisuke Miyazaki, Masahiko Watanabe, Yuka Sato, Shigeo Okabe, Kazuo Kitamura, Masanobu Kano, Kouichi Hashimoto, Hidenori Suzuki, Toru Takumi

  2017年06月, SCIENCE ADVANCES, 3(6) (6), e1603001, 英語

  [査読有り]

  研究論文（学術雑誌）


• Translocated in liposarcoma regulates the distribution and function of mammalian enabled, a modulator of actin dynamics

  Tomohito Sugiura, Shuji Matsuda, Satoshi Kurosaka, Nobuhiro Nakai, Keita Fukumoto, Tetsuya Takahashi, Hirofumi Maruyama, Kazunori Imaizumi, Masayasu Matsumoto, Toru Takumi

  2016年04月, FEBS JOURNAL, 283(8) (8), 1475 - 1487, 英語

  [査読有り]

  研究論文（学術雑誌）


• Neuroanatomical Phenotypes Are Consistent With Autism-Like Behavioral Phenotypes in the 15q11-13 Duplication Mouse Model

  Jacob Ellegood, Nobuhiro Nakai, Jin Nakatani, Mark Henkelman, Toru Takumi, Jason Lerch

  2015年10月, AUTISM RESEARCH, 8(5) (5), 545 - 555, 英語

  [査読有り]

  研究論文（学術雑誌）


• Autism spectrum disorder model mice: Focus on copy number variation and epigenetics

  Nobuhiro Nakai, Susumu Otsuka, Jihwan Myung, Toru Takumi

  2015年10月, SCIENCE CHINA-LIFE SCIENCES, 58(10) (10), 976 - 984, 英語

  [査読有り]


• Clustering autism: using neuroanatomical differences in 26 mouse models to gain insight into the heterogeneity

  J. Ellegood, E. Anagnostou, B. A. Babineau, J. N. Crawley, L. Lin, M. Genestine, E. DiCicco-Bloom, J. K. Y. Lai, J. A. Foster, O. Penagarikano, D. H. Geschwind, L. K. Pacey, D. R. Hampson, C. L. Laliberte, A. A. Mills, E. Tam, L. R. Osborne, M. Kouser, F. Espinosa-Becerra, Z. Xuan, C. M. Powell, A. Raznahan, D. M. Robins, N. Nakai, J. Nakatani, T. Takumi, M. C. van Eede, T. M. Kerr, C. Muller, R. D. Blakely, J. Veenstra-VanderWeele, R. M. Henkelman, J. P. Lerch

  2015年02月, MOLECULAR PSYCHIATRY, 20(1) (1), 118 - 125, 英語

  [査読有り]

  研究論文（学術雑誌）


• 3D visualization of the regional differences.

  Ellegood J, Anagnostou E, Babineau BA, Crawley JN, Lin L, Genestine M, DiCicco-Bloom E, Lai JK, Foster JA, Peñagarikano O, Geschwind DH, Pacey LK, Hampson DR, Laliberté CL, Mills AA, Tam E, Osborne LR, Kouser M, Espinosa-Becerra F, Xuan Z, Powell CM, Raznahan A, Robins DM, Nakai N, Nakatani J, Takumi T, van Eede MC, Kerr TM, Muller C, Blakely RD, Veenstra-VanderWeele J, Henkelman RM, Lerch JP

  2015年02月, Molecular psychiatry, 20(1) (1), 1

  [査読有り]


• Towards understanding the neural mechanism of behavioral phenotypes seen in psychiatric disorders

  Nobuhiro Nakai, Ofer Yizhar, Toru Takumi

  Springer Japan, 2015年01月, Optogenetics: Light-Sensing Proteins and their Applications, 331 - 340, 英語

  [査読有り]

  論文集(書籍)内論文


• 自閉症ヒト型モデルマウスの開発

  玉田 紘太, 中井 信裕, 内匠 透

  著者等が作製した自閉症モデルマウスを中心に、最近の自閉症モデルマウスを紹介した。著者等は、自閉症患者で最も高頻度に発生しているヒト染色体15q11-13領域の重複に注目し、15q重複マウスを作製した。自閉症の三つの主症状に対応する行動試験を含めた網羅的行動解析、セロトニン(5-HT)の関与など神経化学的解析を行った。また、5-HTTノックアウトマウスとの関連性を評価した。

  (公社)日本生化学会, 2011年09月, 生化学, 83(9) (9), 841 - 845, 日本語


• ヒト染色体15q11-13重複モデルマウスにおける興奮・抑制性神経の形態学的解析

  中井 信裕, 渡辺 康仁, 都甲 めぐみ, 廣木 遥, 三嶋 亮, 笹西 美和子, 高橋 哲也, 松本 昌泰, 玉田 紘太, 内匠 透

  (一社)日本解剖学会, 2011年03月, 解剖学雑誌, 86(1) (1), 18 - 18, 日本語


• ヒト型マウスモデルによる自閉症の病態解明と新規治療薬開発の基盤研究

  内匠 透, 玉田 紘太, 友永 省三, 畠中 史幸, 中井 信裕

  (公財)先進医薬研究振興財団, 2011年03月, 精神薬療研究年報, (43) (43), 53 - 54, 日本語


• A humanized mouse model of autism

  Kota Tamada, Nobuhiro Nakai, Toru Takumi

  2011年, Seikagaku, 83(9) (9), 841 - 845, 日本語

  [査読有り]

  研究論文（学術雑誌）


• Decreased Exploratory Activity in a Mouse Model of 15q Duplication Syndrome; Implications for Disturbance of Serotonin Signaling

  Kota Tamada, Shozo Tomonaga, Fumiyuki Hatanaka, Nobuhiro Nakai, Keizo Takao, Tsuyoshi Miyakawa, Jin Nakatani, Toru Takumi

  2010年12月, PLOS ONE, 5(12) (12), e15126, 英語

  [査読有り]

  研究論文（学術雑誌）


• 疾患エピジェネティクスの最前線 インプリンティング領域であるヒト染色体15q11-13相同領域重複マウスの解析

  玉田 紘太, 中谷 仁, 畠中 史幸, 中井 信裕, 大塚 晋, 内匠 透

  (公社)日本生化学会, 2010年12月, 日本生化学会大会・日本分子生物学会年会合同大会講演要旨集, 83回・33回, 4W8 - 6, 日本語


• 染色体工学を用いて作製したヒト染色体15q11-13相同領域重複マウスの行動および脳内モノアミン解析

  玉田 紘太, 友永 省三, 畠中 史幸, 中井 信裕, 高雄 啓三, 宮川 剛, 内匠 透

  (公社)日本生化学会, 2010年12月, 日本生化学会大会・日本分子生物学会年会合同大会講演要旨集, 83回・33回, 2T4 - 10, 日本語


• 染色体工学による自閉症モデルマウスを用いた病態解明及びセロトニン系薬剤の関連研究

  内匠 透, 玉田 紘太, 畠中 史幸, 渡辺 康仁, 中井 信裕, 大塚 晋

  (公財)先進医薬研究振興財団, 2010年03月, 精神薬療研究年報, (42) (42), 53 - 54, 日本語


• Fezf1 Is Required for Penetration of the Basal Lamina by Olfactory Axons to Promote Olfactory Development

  Yasuhito Watanabe, Kiyoshi Inoue, Ayako Okuyama-Yamamoto, Nobuhiro Nakai, Jin Nakatani, Ken-Ichi Nibu, Naoko Sato, Yasuhiko Iiboshi, Kosuke Yusa, Gen Kondoh, Junji Takeda, Toshio Terashima, Toru Takumi

  2009年08月, JOURNAL OF COMPARATIVE NEUROLOGY, 515(5) (5), 565 - 584, 英語

  [査読有り]

  研究論文（学術雑誌）


• 染色体工学を用いて構築した自閉症モデルマウスを利用したセロトニン系薬剤の効用研究

  内匠 透, 玉田 紘太, 畠中 史幸, 友永 省三, 渡辺 康仁, 中井 信裕, Jha Amrendra, 松原 千明, 坪井 節子, 須藤 智美, 岩本 和也, 加藤 忠史, 中谷 仁

  (公財)先進医薬研究振興財団, 2009年03月, 精神薬療研究年報, (41) (41), 63 - 64, 日本語

• マウスを用いた自閉症の研究 (特集 こころの動物モデル : サカナからサルまで)

  石井 宏茂, 中井 信裕, 坪井 貴司, 内匠 透

  先端医学社, 2016年04月, 分子精神医学, 16(2) (2), 91 - 96, 日本語


• マウスを用いた自閉症の研究

  石井宏茂, 中井信裕, 坪井貴司, 内匠透

  2016年, 分子精神医学, (16) (16), 19 - 24, 日本語

  記事・総説・解説・論説等（学術雑誌）


• ニューラルサーキットジェネティクスによる自閉症研究 (特集 自閉症の生物学)

  中井 信裕, 九里 信夫, 内匠 透

  学研メディカル秀潤社 ; 1982-, 2015年, 細胞工学, 34(5) (5), 476 - 482, 日本語


• 自閉症責任領域であるヒト染色体15q11-13領域重複マウスの解析

  玉田紘太, 友永省三, 畠中史幸, 中井信裕, 内匠透

  2011年09月, 日本神経科学学会, 日本語

  研究発表ペーパー・要旨（全国大会，その他学術会議）


• Analysis of chromosome engineered mouse model of 15q duplication

  Kota Tamada, Shozo Tomonaga, Fumiyuki Hatanaka, Nobuhiro Nakai, Toru Takumi

  2011年, NEUROSCIENCE RESEARCH, 71, E75 - E76, 英語

  研究発表ペーパー・要旨（国際会議）

• 自閉症の生物学 監修: 内匠 透

  中井 信裕, 九里 信夫, 内匠 透

  分担執筆, ニューラルサーキットジェネティクスによる自閉症研究, 細胞工学, 2015年


• Optogenetics, Editors: Yawo H, Kandori H, Koizumi A

  Nobuhiro Nakai, Ofer Yizhar, Toru Takumi

  分担執筆, Towards Understanding the Neural Mechanism of Behavioral Phenotypes Seen in Psychiatric Disorders, Springer Japan, 2015年


• オプトジェネティクス-光工学と遺伝学による行動制御技術の最前線—

  中井 信裕, 内匠 透

  分担執筆, オプトジェネティクスを用いた異常行動の神経メカニズムの解明, エヌ・ティー・エス, 2013年


• 疾患モデルマウス表現型解析指南 山村研一、若菜茂晴編

  中井 信裕, 内匠 透

  分担執筆, 発達障害, 中山書店, 2011年

• VRで脳と行動をつなぐ ～自閉症モデルマウスがマウスアバターと出会うとき～

  中井 信裕, 鈴木 真生, 内匠 透

  日本発達神経科学会第14回学術集会, 2025年11月

  [招待有り]

  シンポジウム・ワークショップパネル（指名）


• VR-based real-time imaging system for monitoring and manipulating cortical network dynamics in ASD model mice

  Nobuhiro Nakai

  2025 Peking University Health Science Conferences on Autism Spectrum Disorders, 2025年10月, 英語

  [招待有り]

  口頭発表（招待・特別）


• Cortical network dynamics at locomotion onset in a mouse model of neurodevelopmental disorder

  Nobuhiro Nakai

  APPW2025, 2025年03月

  シンポジウム・ワークショップパネル（公募）


• A mouse VR system for monitoring cortical functional network dynamics during behavior

  Nobuhiro Nakai

  The 101st Annual Meeting of The Physiological Society of Japan, 2024年03月, 英語

  シンポジウム・ワークショップパネル（公募）


• VRシステムを用いた行動時皮質機能ネットワーク動態の解析

  中井 信裕

  生理研研究会2021「行動の多様性を支える神経基盤とその動作様式の解明」, 2022年01月

  [招待有り]


• Cortical network dynamics reflect transitions between locomotor states in head-fixed mice in a virtual reality system

  Nakai N, Sekine Y, Sato M, Takumi T

  Neuroscience 2019, 2019年10月


• 自閉症モデルマウスにおけるセロトニンと脳機能発達

  中井信裕、永野昌俊、齋藤文仁、鈴木秀典、内匠透

  令和元年度生理研研究会 情動研究会, 2019年09月

  [招待有り]


• Development of a virtual reality system for analysis of behavior state-dependent cortical network dynamics in mice

  Nakai N, Sekine Y, Sato M, Takumi T

  The 42nd Annual Meeting of the Japan Neuroscience Society, 2019年07月

  口頭発表（一般）


• 行動状態に基づく脳機能ネットワーク解析のためのマウス用バーチャルリアリティシステム

  中井信裕

  立命館大学システム視覚科学研究センターセミナー, 2019年03月

  [招待有り]


• 脳機能解析のためのマウス行動課題用バーチャルリアリティシステム開発

  中井信裕、佐藤正晃、内匠透

  平成30年度文部科学省新学術領域研究 学術研究支援基盤形成 先端モデル動物支援プラットフォーム, 2019年02月


• A VR system for visualization of behavior-based cortical network in head-fixed mice

  Nakai N, Sato M, Takumi T

  Cold Spring Harbor Asia, the Conference on Latest Advances in Development & Function of Neuronal Circuits, 2018年


• 自閉症モデルマウスの皮質E/Iバランス異常と社会性行動におけるセロトニン調節機能の解析

  Nakai N, Nagano M, Saitow F, Watanabe Y, Kawamura Y, Tamada K, Mizuma H, Onoe H, Monai H, Hirase H, Miyazaki T, Watanabe M, Okabe S, Kano M, Hashimoto K, Suzuki H, Takumi T

  第40回日本神経科学大会, 2017年, 国際会議


• Serotonin rebalances cortical tuning and behavior linked to autism symptoms in 15q11-13 duplication mice

  Nakai N, Nagano M, Saitow F, Watanabe Y, Kawamura Y, Tamada K, Mizuma H, Onoe H, Monai H, Hirase H, Miyazaki T, Watanabe M, Okabe S, Kano M, Hashimoto K, Suzuki H, Takumi T

  SFN2017, 2017年, 国際会議


• A virtual reality paradigm for testing social interaction in head-fixed mice.

  中井 信裕, 佐藤 正晃, 林 康紀, 内匠 透

  第39回日本神経科学大会, 2016年, 国際会議

  ポスター発表


• Cortical excitatory/inhibitory imbalance in a model mouse for human 15q11-13 duplication

  中井 信裕, 河村 吉信, 渡辺 康仁, 宮崎 太輔ら

  第38回日本神経科学大会, 2015年, 国際会議

  ポスター発表


• Excitatory/inhibitory imbalance in a model mouse for human 15q11-13 duplication seen in autism

  N. Nakai, Y. Watanabe, K. Hashimoto, T. Takumi

  Cell symposia, 2013年11月, 英語, 国際会議

  ポスター発表


• 染色体工学を用いて作製したヒト染色体15q11-13相同領域重複マウスの行動および脳内モノアミン解析

  玉田紘太, 友永省三, 畠中史幸, 中井信裕, 高雄啓三, 宮川剛, 内匠透

  BMB2010, 2010年12月, 日本語

  口頭発表（一般）


• ヒト染色体15q11-13重複モデルマウスの興奮・抑制性神経の形態学的解析

  中井信裕

  日本解剖学会 中国・四国支部学術集会, 2010年10月, 日本語, 国内会議

  口頭発表（一般）

• 日本生理学会

  2023年 - 現在


• 日本神経科学学会

• 社会刺激に対する自閉症モデルマウスの立体的皮質機能ネットワーク解析

  中井 信裕

  日本学術振興会, 科学研究費助成事業, 基盤研究(C), 神戸大学, 2025年04月01日 - 2028年03月31日


• マウスメタバース社会空間における当事者化の脳・行動解析

  中井 信裕

  日本学術振興会, 科学研究費助成事業, 学術変革領域研究(A), 神戸大学, 2024年04月01日 - 2026年03月31日


• 社会性神経回路と自閉スペクトラム症におけるその障害

  内匠 透, 中井 信裕, 棒田 亜耶花

  日本学術振興会, 科学研究費助成事業, 国際共同研究加速基金(海外連携研究), 神戸大学, 2023年09月08日 - 2026年03月31日


• ホログラフィック顕微鏡による脳の揺らぎ操作

  中井 信裕

  日本学術振興会, 科学研究費助成事業, 学術変革領域研究(A), 神戸大学, 2023年04月01日 - 2025年03月31日


• 自閉症における感覚モダリティの皮質機能ネットワーク解析

  中井 信裕

  日本学術振興会, 科学研究費助成事業, 若手研究, 神戸大学, 2023年04月01日 - 2025年03月31日


• バーチャルリアリティを用いたマウス社会性行動の感覚モダリティ解析

  中井 信裕

  日本学術振興会, 科学研究費助成事業, 若手研究, 2019年04月01日 - 2023年03月31日

  動物の社会性行動では視覚、聴覚、嗅覚などを含む複数の感覚モダリティが生じ、大脳皮質で統合・処理された感覚情報を基にして特定の行動が表出されると考えられている。しかし、複雑に絡み合った感覚モダリティの存在下では大脳皮質の神経活動様式から行動を読み解くことは難しい。そのため本研究では、バーチャルリアリティ（ＶＲ）システムを用い、現実世界では区別することが困難な社会性刺激を選択的に提示し、行動中マウスに対する感覚モダリティを操作することで、社会性行動時の大脳皮質機能ネットワークの情報処理過程を明らかにする。 二個体の被験マウスが同一のバーチャル空間を自由探索することのできるインタラクティブ型ソーシャルＶＲシステムを用い、視覚、嗅覚、触覚の多感覚な社会刺激条件下、また、個別の感覚刺激条件下の社会性行動と大脳皮質活動を測定した。感覚刺激の組み合わせ条件によって大脳皮質活動がどのように変化するかを解析した。今後も実験数を増やし、解析を進めることで、社会行動関連脳機能ネットワークを同定する。 また、VRシステムを用いて自閉症モデルマウスの行動および大脳皮質機能ネットワークを解析した。野生型マウスとの比較から自閉症特有の大脳皮質機能ネットワークパターンを同定した。本成果は論文にまとめており、現在投稿中である。 国際学会にて、社会性行動を模したバーチャルリアリティ（ＶＲ）実験系による脳機能ネットワーク解析法および自閉症モデルマウスの機能ネットワーク異常をシンポジウムで口頭発表した。