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Chronic fluoxetine treatment improves ischemia‐induced spatial cognitive deficits through increasing hippocampal neurogenesis after stroke
Author(s) -
Li WenLei,
Cai HuiHui,
Wang Bin,
Chen Ling,
Zhou QiGang,
Luo ChunXia,
Liu Na,
Ding XinSheng,
Zhu DongYa
Publication year - 2009
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.21829
Subject(s) - neurogenesis , hippocampal formation , fluoxetine , hippocampus , dentate gyrus , neuroscience , memory impairment , psychology , ischemia , serotonin reuptake inhibitor , stroke (engine) , brain ischemia , cognition , medicine , serotonin , psychiatry , antidepressant , mechanical engineering , receptor , engineering
Cognitive deficits, including spatial memory impairment, are very common after ischemic stroke. Neurogenesis in the dentate gyrus (DG) contributes to forming spatial memory in the ischemic brain. Fluoxetine, a selective serotonin reuptake inhibitor, can enhance neurogenesis in the hippocampus in physiological situations and some neurological diseases. However, whether it has effects on ischemia‐induced spatial cognitive impairment and hippocampal neurogenesis has not been determined. Here we report that fluoxetine treatment (10 mg kg −1 , i.p.) for 4 weeks promoted the survival of newborn cells in the ischemic hippocampus and, consequently, attenuated spatial memory impairment of mice after focal cerebral ischemia. Disrupting hippocampal neurogenesis blocked the beneficial effect of fluoxetine on ischemia‐induced spatial cognitive impairment. These results suggest that chronic fluoxetine treatment benefits spatial cognitive function recovery following ischemic insult, and the improved cognitive function is associated with enhanced newborn cell survival in the hippocampus. Our results raise the possibility that fluoxetine can be used as a drug to treat poststroke spatial cognitive deficits. © 2008 Wiley‐Liss, Inc.