Fluoxetine increases the activity of the ERK-CREB signal system and alleviates the depressive-like behavior in rats exposed to chronic forced swim stress.
作者： Xiaoli Qi , Wenjuan Lin , Junfa Li , Huanhuan Li , Weiwen Wang
DOI: 10.1016/J.NBD.2008.05.003
关键词: Kinase 、 CREB 、 Antidepressant 、 MAPK/ERK pathway 、 Prefrontal cortex 、 Internal medicine 、 Extracellular 、 Psychology 、 Fluoxetine 、 Hippocampus 、 Endocrinology
摘要: Our previous research indicates that the extracellular signal-regulated kinase (ERK)-cyclic AMP-responsive-element-binding protein (CREB) signal system may be involved in molecular mechanism of depression. The present study further investigated effect antidepressant fluoxetine on ERK-CREB and depressive-like behaviors rats. Fluoxetine was administrated to either naive rats or stressed for 21 days. results showed chronic forced swim stress induced decreased levels P-ERK2, P-CREB, ERK1/2 CREB hippocampus prefrontal cortex. alleviated reversed disruptions P-ERK2 P-CREB also exerted mood-elevating increased These suggest targets action participate neuronal
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