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Aim To investigate the mechanisms underlying depressivelike behavior induced by chronic cerebral ischemia in rats.Methods In the present study, a chronic cerebral hypoperfusion model was established by permanent bilateral common carotid arteries occlusion (twovessel occlusion, 2VO) in rats.Two weeks after 2VO, GABAB receptor agonist baclofen (25 mg· kg1 · d1 , i.p.) was administrated for 21 days.The FST was performed to evaluate depressivelike 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 obvious depressivelike behavior in rats.Activation of GABAB receptors alleviates the depressivelike behavior induced by chronic cerebral ischemia via upredulation of BDNF in hippocampal CA1 in rats.