Activation of GABAB receptors alleviates depressive-like behavior induced by chronic cerebral ischemia via upredulation of BDNF in rats

摘要

Aim To investigate the mechanisms underlying depressive-like behavior induced by chronic cerebral is- chemia in rats. Methods In the present study, a chronic cerebral hypoperfusion model was established by perma- 2VO） in rats. Two weeks after 2VO, GAB- nent bilateral common carotid arteries occlusion （two-vessel occlusion, AB receptor agonist baclofen （25 mg · kg^-1 . d^-1 i p ） was administrated for 21 days. The FST was performed to evaluate depressive-like behavior in which the immobility time was recorded. In addition, the expression of brain derived neurotrophic factor （BDNF） in hippocampal CA1 was measured by Western blot. Results The immobility time of 2VO group was significantly prolonged and the expression of BDNF was decreased by 28.95% compared with sham group. After activation of GABAB receptors by baclofen, the immobility time was significantly reduced and the expression of BDNF was increased by 47.91% compared with 2VO group. Conclusion 2VO induced ob- vious depressive-like behavior in rats. Activation of GABAB receptors alleviates the depressive-like behavior in- duced by chronic cerebral ischemia via upredulation of BDNF in hippocampal CA1 in rats.