Neural mechanism of tic disorders revealed by optical imaging in the brain

2020 Fiscal Year Final Research Report

• Project/Area Number: 18K06852
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 48020:Physiology-related
• Research Institution: Kobe University
• Principal Investigator: Tachibana Yoshihisa 神戸大学, 医学研究科, 准教授 (50373197)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: 大脳基底核 / 線条体 / GABA / 不随意運動 / 情動

Outline of Final Research Achievements

The pathophysiology of motor and vocal tics remains unknown. Recently, the disinhibition of the striatum is suggested to cause the tic symptoms. To test this issue, we unilaterally injected GABA antagonist bicuculline into the mouse striatum. We found that the local bicuculline into the striatum induced contralateral muscle twitches depending on injection sites. Then, we investigated the activated brain regions by striatal disinhibition using c-Fos immunohistochemistry. We found that limbic structures such as the amygdala, cingulate cortex, insular cortex as well as the primary motor cortex were activated although the structure does not receive direct inputs from the striatum. These data suggest that the tic is generated by abnormal neuronal processing in the motor-limbic network in the brain.

Free Research Field

神経科学

Academic Significance and Societal Importance of the Research Achievements

トゥレット症候群に代表されるように、運動チックや音声チックを患い、薬物療法、認知行動療法が奏功しない患者が数多くいる。その理由として、チック症の神経生理学的な病態メカニズムが明らかになっていないことが挙げられる。本研究において、大脳基底核の機能異常を起因とし、情動と運動をつなぐ神経ネットワークの情報処理の異常からチック症状が惹起されうることが明らかとなった。本研究成果は、生活上の困難さやハンディキャップを持ったまま社会生活を送らざるをえないチック症患者にとって、症状を緩和させる新たな治療法の開発に大いに役立つと期待される。