Imipramine-Induced c-Fos Expression in the Medial Prefrontal Cortex is Decreased in the ACTH-Treated Rats

被引:16
作者
Li, Bingjin [1 ,3 ]
Suemaru, Katsuya [2 ,3 ]
Kitamura, Yoshihisa [4 ]
Gomita, Yutaka [2 ]
Araki, Hiroaki [3 ]
Cui, Ranji [1 ,3 ]
机构
[1] NE Normal Univ, Sch Life Sci, Changchun 130024, Peoples R China
[2] Shujitsu Univ, Sch Pharm, Okayama 7038516, Japan
[3] Ehime Univ, Sch Med, Div Hosp Pharm, Matsuyama, Ehime 7910295, Japan
[4] Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Pharmaceut Care & Hlth Sci, Okayama 7008530, Japan
关键词
Cell; c-Fos; Depression; Medial Prefrontal cCrtex; TREATMENT-RESISTANT DEPRESSION; CENTRAL EXTENDED AMYGDALA; ANTIDEPRESSANT DRUGS; RECEPTOR-BINDING; 5-HT2A RECEPTOR; STRESS; BRAIN; MOOD; DESMETHYLIMIPRAMINE; IMMUNOREACTIVITY;
D O I
10.1002/jbt.21510
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Previous studies have shown that the antidepressive-like effect of tricyclic antidepressants is blocked by repeated treatments with adrenocorticotropic hormone (ACTH). However, little is known about the neuroanatomy underlying the mechanism of the imipramine treatment-resistant depression model. In the present study, first experimental evidence showed no significant difference of the serum imipramine concentrations between the saline and ACTH-treated rats. In further study, imipramine produced significant increases in the c-Fos expression in the medial prefrontal cortex (mPFC), the dentate gyrus of the hippocampus (DGH), and the central nucleus of the amygdala (CeA), in rats repeatedly treated with saline. The imipramine-increased c-Fos immunoreactivity was suppressed in the mPFC of rats repeatedly treated with ACTH. However, there was no significant difference in c-Fos expression in the DGH and CeA between ACTH- and saline-treated rats. These results suggest that the mPFC is maybe involved in effects of the imipramine in the ACTH-treated rats. (c) 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:486-491, 2013; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.21510
引用
收藏
页码:486 / 491
页数:6
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