Abstract

The purpose of this study was to discuss the effect of voluntary wheel running on striatal dopamine levels and anxiety-like behavior in rats with global cerebral ischemia. The male Sprague-Dawley rats were signed on in this study and randomly divided into following 4 groups: Control group (C group), Sham group (S group), ischemia group (I group), and 3 weeks physical exercise before ischemia group (3RI group). The rats in the 3RI group were placed in a voluntary running wheel for three weeks to exercise. Then, the rats in I and 3RI groups received bilateral carotid artery ligation (2-VO) operation. The C and S group did not perform voluntary running exercise and the bilateral common carotid arteries of S group were exposed without ligation. In vivo microdialysis was used in conjunction with high performance liquid chromatography (HPLC) and electrochemical detection to ascertain the level of dopamine in the striatum. Elevated plus maze (EPM) and open field (OF) were used to test anxiety status at 24 hours and 7days after 2-VO cerebral ischemia. Meanwhile, gait and motor coordination evaluations were carried out to eliminate the influence of non-specific motor problems. The results indicated that cerebral ischemia instigate the increase of striatal dopamine in I group rats during acute cerebral ischemia. A 3-week voluntary wheel running significantly enhances the striatal dopamine before ischemia and obstructs a further increase of dopamine during acute cerebral ischemia in 3RI group rats. At 24 hours after ischemia, striatal dopamine returned to pre-ischemic levels in 3RI group. Striatal dopamine in I group were less than pre-ischemic levels at 7 days. Behavioral data indicated that 3-week voluntary wheel running promoted recovery of anxiety-like behavior and gait were not affected by 2-VO cerebral ischemia at 24 hours post-ischemia rats. Therefore, it can be concluded that 3-week physical exercise significantly increased the striatal dopamine and improved anxiety-like behavior by inhibiting the increase of dopamine during acute cerebral ischemia and suppressing the decrease of dopamine after 24 hours and 7 days cerebral ischemia.

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