Literature DB >> 22658339

Chronic clomipramine treatment restores hippocampal expression of glial cell line-derived neurotrophic factor in a rat model of depression.

Qiong Liu1, Hai-Yan Zhu, Bing Li, Yan-Qing Wang, Jin Yu, Gen-Cheng Wu.   

Abstract

BACKGROUND: Because there is evidence that certain neurotrophic factors are involved in depression and the mechanism of antidepressant treatment, it is hypothesized that neurotrophic factors may also play a functional role in the etiology of depression and treatment. Glial cell line-derived neurotrophic factor (GDNF) is a member of the transforming growth factor (TGF-β)-super-family. We performed a study to assess the impact of chronic unpredictable stress (CUS) and clomipramine treatment on GDNF expression in the rat hippocampus.
METHOD: Using a rat model of CUS-induced depression, we administered clomipramine, one of the typical antidepressants, every day for 3 weeks starting 2 weeks after the beginning of the experiment. GDNF level in the hippocampus was detected by immunohistochemsitry, Western blot analysis, and reverse transcription-polymerase chain reaction (RT-PCR). Behavioral changes were measured by forced swimming test (FST) and open field test (OFT).
RESULTS: Animals exposed to CUS showed depression-like behavior and exhibited a significant decrease in GDNF expression in the hippocampus. Chronic clomipramine treatment reversed the behavioral deficits and the decrease in GDNF levels induced by CUS. LIMITATION: The relatively small number of the depression-model rats may cause some bias of behavioral tests.
CONCLUSION: In our study, chronic clomipramine treatment restored GDNF expression in the hippocampus of CUS-induced depression rats, suggesting that GDNF is involved in the behavioral responses to antidepressants. The beneficial effects of clomipramine suggest that GDNF may be a viable target for new antidepressant drug development.
Copyright © 2012 Elsevier B.V. All rights reserved.

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Year:  2012        PMID: 22658339     DOI: 10.1016/j.jad.2012.03.018

Source DB:  PubMed          Journal:  J Affect Disord        ISSN: 0165-0327            Impact factor:   4.839


  17 in total

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