精神・神経病態解明センター準備室

Hiromi Sano

  (佐野 裕美)

Profile Information

Affiliation
Associate Professor, International Center for Brain Science, Fujita Health University

J-GLOBAL ID
200901066461385086
researchmap Member ID
5000043571

Papers

 36
  • Nozomu Yoshioka, Masayuki Kurose, Hiromi Sano, Dang Minh Tran, Satomi Chiken, Kazuki Tainaka, Kensuke Yamamura, Kenta Kobayashi, Atsushi Nambu, Hirohide Takebayashi
    Science Advances, 10(30), Jul 26, 2024  
    Mutations in Dystonin ( DST ), which encodes cytoskeletal linker proteins, cause hereditary sensory and autonomic neuropathy 6 (HSAN-VI) in humans and the dystonia musculorum ( dt ) phenotype in mice; however, the neuronal circuit underlying the HSAN-VI and dt phenotype is unresolved. dt mice exhibit dystonic movements accompanied by the simultaneous contraction of agonist and antagonist muscles and postnatal lethality. Here, we identified the sensory-motor circuit as a major causative neural circuit using a gene trap system that enables neural circuit-selective inactivation and restoration of Dst by Cre-mediated recombination. Sensory neuron–selective Dst deletion led to motor impairment, degeneration of proprioceptive sensory neurons, and disruption of the sensory-motor circuit. Restoration of Dst expression in sensory neurons using Cre driver mice or a single postnatal injection of Cre-expressing adeno-associated virus ameliorated sensory degeneration and improved abnormal movements. These findings demonstrate that the sensory-motor circuit is involved in the movement disorders in dt mice and that the sensory circuit is a therapeutic target for HSAN-VI.
  • Atsushi Nambu, Satomi Chiken, Hiromi Sano, Nobuhiko Hatanaka, José A. Obeso
    Rinsho Shinkeigaku, 64(6) 390-397, 2024  
  • Yuri Miyazaki, Takeshi Otsuka, Yoko Yamagata, Toshihiro Endo, Makoto Sanbo, Hiromi Sano, Kenta Kobayashi, Hiroki Inahashi, Hans-Christian Kornau, Dietmar Schmitz, Harald Prüss, Dies Meijer, Masumi Hirabayashi, Yuko Fukata, Masaki Fukata
    Cell Reports, 113634-113634, Jan, 2024  
  • Atsushi Nambu, Satomi Chiken, Hiromi Sano, Nobuhiko Hatanaka, José A Obeso
    Movement disorders : official journal of the Movement Disorder Society, 38(12) 2145-2150, Dec, 2023  
    Schematic illustration of cortically induced dynamic activity changes of the output nuclei of the basal ganglia (the internal segment of the globus pallidus, GPi and the substantia nigra pars reticulata, SNr) in the healthy and diseased states. The height of the dam along the time course controls the expression of voluntary movements. Its alterations could cause a variety of movement disorders, such as Parkinson's disease and hyperkinetic disorders. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
  • Yoshifumi Abe, Sho Yagishita, Hiromi Sano, Yuki Sugiura, Masanori Dantsuji, Toru Suzuki, Ayako Mochizuki, Daisuke Yoshimaru, Junichi Hata, Mami Matsumoto, Shu Taira, Hiroyoshi Takeuchi, Hideyuki Okano, Nobuhiko Ohno, Makoto Suematsu, Tomio Inoue, Atsushi Nambu, Masahiko Watanabe, Kenji F Tanaka
    Cell reports. Medicine, 101208-101208, Sep 22, 2023  Peer-reviewed
    Dyskinesia is involuntary movement caused by long-term medication with dopamine-related agents: the dopamine agonist 3,4-dihydroxy-L-phenylalanine (L-DOPA) to treat Parkinson's disease (L-DOPA-induced dyskinesia [LID]) or dopamine antagonists to treat schizophrenia (tardive dyskinesia [TD]). However, it remains unknown why distinct types of medications for distinct neuropsychiatric disorders induce similar involuntary movements. Here, we search for a shared structural footprint using magnetic resonance imaging-based macroscopic screening and super-resolution microscopy-based microscopic identification. We identify the enlarged axon terminals of striatal medium spiny neurons in LID and TD model mice. Striatal overexpression of the vesicular gamma-aminobutyric acid transporter (VGAT) is necessary and sufficient for modeling these structural changes; VGAT levels gate the functional and behavioral alterations in dyskinesia models. Our findings indicate that lowered type 2 dopamine receptor signaling with repetitive dopamine fluctuations is a common cause of VGAT overexpression and late-onset dyskinesia formation and that reducing dopamine fluctuation rescues dyskinesia pathology via VGAT downregulation.

Misc.

 13

Research Projects

 7