Fluoxetine increases the activity of the ERK-CREB signal system and alleviates the depressive-like behavior in rats exposed to chronic forced swim stress
Qi, Xiaoli1; Lin, Wenjuan1; Li, Junfa2; Li, Huanhuan1; Wang, Weiwen1; Wang, Donglin1; Sun, Meng1; Wenjuan Lin
2008-08-01
发表期刊NEUROBIOLOGY OF DISEASE
ISSN0969-9961
文章类型Article
卷号31期号:2页码:278-285
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 the molecular mechanism of depression. The present study further investigated the effect of antidepressant fluoxetine on the ERK-CREB signal system and the depressive-like behaviors in rats. Fluoxetine was administrated to either naive rats or stressed rats for 21 days. The results showed that chronic forced swim stress induced depressive-like behaviors and decreased the levels of P-ERK2, P-CREB, ERK1/2 and CREB in hippocampus and prefrontal cortex. Fluoxetine alleviated the depressive-like behaviors and reversed the disruptions of the P-ERK2 and P-CREB in stressed rats. Fluoxetine also exerted mood-elevating effect and increased the levels of the P-ERK2 and P-CREB in naive rats. These results suggest that the ERK-CREB signal system may be the targets of the antidepressant action of fluoxetine and participate in the neuronal mechanism of depression.; Our previous research indicates that the extracellular signal-regulated kinase (ERK)-cyclic AMP-responsive-element-binding protein (CREB) signal system may be involved in the molecular mechanism of depression. The present study further investigated the effect of antidepressant fluoxetine on the ERK-CREB signal system and the depressive-like behaviors in rats. Fluoxetine was administrated to either naive rats or stressed rats for 21 days. The results showed that chronic forced swim stress induced depressive-like behaviors and decreased the levels of P-ERK2, P-CREB, ERK1/2 and CREB in hippocampus and prefrontal cortex. Fluoxetine alleviated the depressive-like behaviors and reversed the disruptions of the P-ERK2 and P-CREB in stressed rats. Fluoxetine also exerted mood-elevating effect and increased the levels of the P-ERK2 and P-CREB in naive rats. These results suggest that the ERK-CREB signal system may be the targets of the antidepressant action of fluoxetine and participate in the neuronal mechanism of depression. (C) 2008 Elsevier Inc. All rights reserved.
关键词ERK CREB stress antidepressant hippocampus prefrontal cortex
学科领域生理心理学/生物心理学
收录类别SCI
语种英语
WOS记录号WOS:000258115700012
引用统计
文献类型期刊论文
条目标识符http://ir.psych.ac.cn/handle/311026/5413
专题中国科学院心理研究所回溯数据库(1956-2010)
通讯作者Wenjuan Lin
作者单位1.Chinese Acad Sci, Inst Psychol, Key Lab Mental Hlth, Beijing 100101, Peoples R China
2.Capital Med Univ, Beijing 100069, Peoples R China
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Qi, Xiaoli,Lin, Wenjuan,Li, Junfa,et al. Fluoxetine increases the activity of the ERK-CREB signal system and alleviates the depressive-like behavior in rats exposed to chronic forced swim stress[J]. NEUROBIOLOGY OF DISEASE,2008,31(2):278-285.
APA Qi, Xiaoli.,Lin, Wenjuan.,Li, Junfa.,Li, Huanhuan.,Wang, Weiwen.,...&Wenjuan Lin.(2008).Fluoxetine increases the activity of the ERK-CREB signal system and alleviates the depressive-like behavior in rats exposed to chronic forced swim stress.NEUROBIOLOGY OF DISEASE,31(2),278-285.
MLA Qi, Xiaoli,et al."Fluoxetine increases the activity of the ERK-CREB signal system and alleviates the depressive-like behavior in rats exposed to chronic forced swim stress".NEUROBIOLOGY OF DISEASE 31.2(2008):278-285.
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