作者: Michelle Ploughman , Shirley Granter-Button , Garry Chernenko , Zachary Attwood , Budd A. Tucker
DOI: 10.1016/J.BRAINRES.2007.02.065
关键词:
摘要: Exercise increases brain-derived neurotrophic factor (BDNF), phosphorylated cAMP response-element binding protein (pCREB), insulin-like growth (IGF-I) and synapsin-I, each of which has been implicated in neuroplastic processes underlying recovery from ischemia. In this study we examined the temporal profile (0, 30, 60 120 min following exercise) these proteins hippocampus sensorimotor cortex both motorized (60 min) voluntary (12 h) running, 2 weeks after focal Our goal was to identify optimal training paradigms (intensity, duration frequency) needed integrate endurance exercise stroke rehabilitation. Therefore utilized telemetry measure changes heart rate with methods. findings show that although more intense, running induced a rapid increase BDNF, elevation short-lived than running. Motorized also associated higher levels synapsin-I several brain regions but simultaneously, pronounced stress hormone, corticosterone. Furthermore, forms resulted decreased phosphorylation CREB downregulation beginning 30 bout. This phenomenon robust method generated serum corticosterone levels. immediate response is likely specific acute may diminish repeated exposure. The present data illustrate complex interaction between different neuroplasticity. For clinical application, frequent lower intensity episodes (as wheels), be safer provide patients stroke, delayed sustained effect on BDNF support remodeling stroke.