Clomipramine treatment reversed the glial pathology in a chronic unpredictable stress-induced rat model of depression

Abstract Growing evidence indicates that glia pathology contributes to the pathophysiology and possibly the etiology of depression. The study investigates changes in behaviors and glial fibrillary associated protein (GFAP) in the rat hippocampus after chronic unpredictable stress (CUS), a rat model...

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Published in:European neuropsychopharmacology 2009-11, Vol.19 (11), p.796-805
Main Authors: Liu, Qiong, Li, Bing, Zhu, Hai-Yan, Wang, Yan-Qing, Yu, Jin, Wu, Gen-Cheng
Format: Article
Language:English
Subjects:
Animals
Clomipramine
Clomipramine - pharmacology
Clomipramine - therapeutic use
Depression
Depression - drug therapy
Depression - etiology
Depression - pathology
Disease Models, Animal
Exploratory Behavior - drug effects
Freezing Reaction, Cataleptic
Gene Expression Regulation - drug effects
GFAP
Glia
Glial Fibrillary Acidic Protein - genetics
Glial Fibrillary Acidic Protein - metabolism
Hippocampus
Hippocampus - drug effects
Hippocampus - pathology
Internal Medicine
Male
Neuroglia - drug effects
Neuroglia - metabolism
Neuroglia - pathology
Psychiatry
Rats
Rats, Sprague-Dawley
RNA, Messenger - metabolism
Serotonin Uptake Inhibitors - pharmacology
Serotonin Uptake Inhibitors - therapeutic use
Stress, Psychological - complications
Swimming
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Summary:Abstract Growing evidence indicates that glia pathology contributes to the pathophysiology and possibly the etiology of depression. The study investigates changes in behaviors and glial fibrillary associated protein (GFAP) in the rat hippocampus after chronic unpredictable stress (CUS), a rat model of depression. Furthermore, we studied the effects of clomipramine, one of tricyclic antidepressants (TCAs), known to modulate serotonin and norepinephrine uptake, on CUS-induced depressive-like behaviors and GFAP levels. Rats exposed to CUS showed behavioral deficits in physical state, open field test and forced swimming test and exhibited a significant decrease in GFAP expression in the hippocampus. Interestingly, the behavioral and GFAP expression changes induced by CUS were reversed by chronic treatment with the antidepressant clomipramine. The beneficial effects of clomipramine treatment on CUS-induced depressive-like behavior and GFAP expression provide further validation of our hypothesis that glial dysfunction contributes to the pathophysiology of depression and that glial elements may represent viable targets for new antidepressant drug development.
ISSN:0924-977X
1873-7862
DOI:10.1016/j.euroneuro.2009.06.010