Imipramine‐Induced c‐Fos Expression in the Medial Prefrontal Cortex is Decreased in the ACTH‐Treated Rats. Issue 11 (6th August 2013)

• Record Type: Journal Article
• Authors: Li, Bingjin; Suemaru, Katsuya; Kitamura, Yoshihisa; Gomita, Yutaka; Araki, Hiroaki; Cui, Ranji
• Is Part Of: Journal of biochemical and molecular toxicology. Volume 27:Issue 11(2013:Nov.)
• Page Start: 486
• Page End: 491
• Publication Date: 2013-08-06
• Subjects: Biochemistry -- Periodicals; Molecular biology -- Periodicals; Toxicology -- Periodicals; 574
• DOI: 10.1002/jbt.21510
• Languages: English
• ISSNs: 1095-6670

Abstract

<abstract abstract-type="main"> <title>ABSTRACT</title> <p>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. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:486‐491, 2013; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.21510</p> </abstract>