Elucidation of cellular and nuclear signals that regulate motor learning

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04254
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Neurophysiology / General neuroscience
• Research Institution: Gunma University
• Principal Investigator: Hirai Hirokazu 群馬大学, 大学院医学系研究科, 教授 (70291086)
• Co-Investigator(Renkei-kenkyūsha): HOSOI Nobutake 群馬大学, 大学院医学系研究科, 講師 (90543570) ; KONNO Ayumu 群馬大学, 大学院医学系研究科, 講師 (40509048)
• Research Collaborator: MATSUZAKI Yasunori 群馬大学, 大学院医学系研究科, 助教 (50738200)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 小脳 / プルキンエ細胞 / mGluR1 / 運動学習 / バクロフェン / 脊髄小脳失調症

Outline of Final Research Achievements

Decrease of several genes including transient receptor potential cation channel type 3 (TRPC3), inositol trisphosphate (IP3) receptor and Homer protein homolog 3 (HOMER3) were found in the cerebellum of spinocerebellar ataxia type 1 (SCA1) knock-in mouse. We identified retinoid-related orphan receptor α (RORα), which is a transcription factor that could regulate expression of those genes. Moreover, we found that a gene “X” is increased more than 3 times in SCA1 knock-in mice 3 h after treatment with baclofen and rotarod training. Since haploinsufficiency of the gene “X” is known to cause mental retardation, upregulation of the gene “X” may play a key role in baclofen-induced improvement of motor learning in SCA1 mice.

Free Research Field

神経生理学、神経科学