The Effects of Antecedent Exercise on Motor Function Recovery and Brain-derived Neurotrophic Factor Expression after Focal Cerebral Ischemia in Rats

Abstract

Abstract. [Purpose] In the present study, we investigated the effect of antecedent exercise on functional recovery and brain-derived neurotrophic factor (BDNF) expression following focal cerebral ischemia injury.[Subjects] The rat middle cerebral artery occlusion (MCAO) model was employed. Adult male Sprague-Dawley rats were randomly divided into 4 groups. Group I included untreated normal rats (n=10); Group II included untreated rats with focal cerebral ischemia (n=10); Group III included rats that performed treadmill exercise (20 m/min) training after focal cerebral ischemia (n=10); and Group IV included rats that performed antecedent treadmill exercise (20 m/min) training before focal cerebral ischemia (n=10) as well as treadmill exercise after ischemia. At different time points (1, 7, 14, and 21 days) Garcia's score, and the hippocampal expressions level of BDNF were examined. [Results] In the antecedent exercise group, improvements in the motor behavior index (Garcia's score) were observed and hippocampal BDNF protein expression levels increased. [Conclusion] These results indicate that antecedent treadmill exercise, before permanent brain ischemia exerts a neuroprotective effect against ischemia brain injury by improving motor performance and increasing the level of BDNF expression. Furthermore, the antecedent treadmill exercise of appropriate intensity is critical for post-stroke rehabilitation.

Treadmill exercise improves memory and increases hippocampal BDNF in a rat model of Alzheimer's Disease

“…It has been reported that up-regulation of BDNF leads to a decrease in Aβinduced neurotoxicity (Doi et al, 2013). Cognition and memory functions are positively affected by brain-derived neurotrophic factor (BDNF) (Kim and Kim, 2013). BDNF is a member of the neurotrophin family of growth factors, which has been expressed in the highest level in the brain especially in the hippocampus and facilitates the release of glutamate and enhances the phosphorylation of the NR1 and NR2B subunits of the NMDA-receptor complex (Tyler and Pozzo-Miller, 2001).…”