Mechanism of hyper activity of motoneuron and effect of rehabilitation in spasticity post-stroke mouse.

2014 Fiscal Year Final Research Report

• Project/Area Number: 25750201
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Rehabilitation science/Welfare engineering
• Research Institution: Nagoya University
• Principal Investigator: LEE Sachiko 名古屋大学, 医学(系)研究科(研究院), 助教 (80599316)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: spasticity / stroke / KCC2 / Ia afferent fibers

Outline of Final Research Achievements

An estimated 42.6%of post-stroke patients exhibit spasticity 6 months post-stroke, and this disrupts their ability to perform activities of daily living and decrease their quality of life. In this study, we uncovered that significant reduction of KCC2 (potassium-chloride cotransporter 2) at 7 d post-stroke and phosphorylation of KCC2 serine residue 940 (S940) at 3 and 7 d post-stroke in motoneuron plasma membranes, since this is the main chloride extruder that affects neuronal excitability. In addition, at 7 and 42 d post-stroke, experimental mice exhibited a significant increase in vGluT1 (vesicular glutamate transporter 1)- positive boutons (almost Ia afferent fibers)compared with sham mice. Our findings suggest that both the down-regulation of KCC2 and increases in La afferent fibers are involved in post-stroke spasticity.

Free Research Field

physical therapy