2010 Fiscal Year Final Research Report
Alteration of functional molecule related to improvement of motor performance in the brain of rats with focal cerebral infarction
| Project/Area Number |
20700443
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Rehabilitation science/Welfare engineering
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| Research Institution | Fujita Health University |
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Principal Investigator |
MIZUTANI Kenmei Fujita Health University, 藤田記念七栗研究所, 助教 (30351068)
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| Project Period (FY) |
2008 – 2010
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| Keywords | リハビリテーション / 脳梗塞モデル / FITプログラム / Antibody microarray / 神経可塑性 |
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| Research Abstract |
Identification of functional molecules in the brain related to improvement of the degree of paralysis or increase of activities will contribute to establishing a new treatment strategy for stroke rehabilitation. Hence, protein expression changes in the cerebral cortex of rat groups with/without voluntary exercise after cerebral infarction were examined in this study. In behavioral evaluation, the mean latency until falling from the rotating rod in the group with voluntary exercise for five days was significantly longer than that in the group without voluntary exercise. The protein expression profile was screened by antibody microarray analysis and was confirmed by Western blotting. Fifteen proteins showed significant quantitative changes in the cerebral cortex adjacent to the infarction area after voluntary exercise for five days compared to rats without exercise. Up-regulated proteins were involved in protein phosphorylation, stress response, cell structure and motility, DNA replication and neurogenesis (11 proteins). In contrast, down-regulated proteins were related to apoptosis, cell adhesion and proteolysis (4 proteins). Additional protein expression analysis showed that both growth-associated protein 43 (GAP43) and phosphorylated serine41 GAP43 (pSer41-GAP43) were significantly increased adjacent to the lesion cortex. These results suggest that alteration of these protein expressions may be related to the underlying mechanisms of exercise-induced paralysis recovery, that is, neurite formation, and remodeling of synaptic connections may be through the interaction of NGF, calmodulin, PKC and GAP43. In the present study at least some of the participation of modulators associated with the improvement of paralysis adjacent to the brain lesion might be detected.
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