Optogenetical analysis of sensory-motor integration in mouse phtothorombosis model

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K16664
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Neurosurgery
• Research Institution: Tokyo Women's Medical University
• Principal Investigator: FUKUI ATSUSHI 東京女子医科大学, 医学部, 助教 (80746800)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: sesory-motor integration / motor cortex / sesnsory cortex / photothrombosis / neuromodulation / mouse / optogenetics

Outline of Final Research Achievements

Motor cortex (M1) infarction occasionally causes sensory impairment. Because sensory signal plays an important role in motor control, sensory impairment compromises recovery and rehabilitation from motor disability. Despite the importance of sensory-motor integration for rehabilitation , the neural mechanism of the sensory impairment is poorly understood. We show that the sensory processing in the primary somatosensory cortex (S1) was impaired in the acute phase of M1 infarction and recovered in a layer-specific manner in the subacute phase. This layer dependent recovery process and the anatomical connection pattern from M1 to S1 suggested the functional connectivity from M1 to S1 plays a key role in the impairment of sensory processing in S1. Consistently,optogenetic activation of M1 suppressed the sustained response in S1.Therefore, we revealed how focal stroke of M1 alters cortical network activity of sensory processing, in which inhibitory input from M1 to S1 may be involved.

Free Research Field

脳神経外科

Academic Significance and Societal Importance of the Research Achievements

脳梗塞によって運動麻痺が出現し、そこからどのような感覚刺激をいれてリハビリテーションを行っていくと、運動機能が改善するかはまだよくわかっていない。今回マウスの光遺伝学的実験によって、運動野の脳梗塞により感覚野への抑制性入力が低下し、感覚刺激に対する時間分解能が低下することを示した。これにより、運動機能改善に必要な感覚入力の適切な時期や方法の理解の進展につながっていくと考えられる。