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Exerc Sci > Volume 21(2); 2012 > Article
Exercise Science 2012;21(2): 255-262. doi: https://doi.org/10.15857/ksep.2012.21.2.255
외상성 뇌 손상 후 운동에 의해 활성화된 BDNF-ERK 신호전달 경로가 소뇌에서 발생된 퍼킨제 세포 사멸과 astrogliosis에 미치는 역할 규명
서태범1, 윤진환2
Studies on exercise-activated BDNF-ERK pathway in Purkinje cell loss and astrogliosis in the cerebellum after forebrain traumatic contusion injury
The cerebellum is selectively vulnerable to forebrain traumatic brain injuries (TBI). Physical exercise in animals has been implicated in promoting cell survival and functional recovery after brain injuries. The purpose of this study is to investigate the effects of exercise-increased BDNF (Brain-derived neurotrophic factor) and p-ERK1/2(phospho-extracular signal-regulated kinase1/ell2) on Purkinje neuron survival and astrogiosis in the gyrus of lobules VIII and IX of the cerebellum after TBI. The rats were divided into three groups:the sham-operation group, the TBI-induction group, and the TBI-induction with exercise group. All tissues were used for immunofluorescence staining and Western blot. Calbindin-positive Purkinje neurons were decreased and GFAP (Glial fibrillary acidic protein)-positive astrocytes were increased in the posterior region of the cerebellum after TBI. Treadmill exercise after TBI significantly upregulated induction levels of calbindin, BDNF and p-ERK1/2 as well as decreased GFAP expression levels in lobules of VIII and IX of the cerebellum after TBI. The present study provides the possibility that treadmill exercise may be an important mediator to prevent Purkinje neuron loss and formation of astrogliosis via activation of BDNF and p-ERK1/2.
Key words: Traumatic brain injury, Treadmill exercise, Purkinje cell, Astrogliosis, BDNF, ERK1/2
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