Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2008 Jan;106(1):100-6.
doi: 10.1254/jphs.fp0071615. Epub 2008 Jan 11.

Increased DOI-induced wet-dog shakes in adrenocorticotropic hormone-treated rats are not affected by chronic imipramine treatment: possible involvement of enhanced 5-HT(2A)-receptor expression in the frontal cortex

Yoshihisa Kitamura  1 , Kazuhiko Shibata, Kozue Akiyama, Shizue Kimoto, Yoshika Fujitani, Kouhei Kitagawa, Hirotaka Kanzaki, Mamoru Ouchida, Kenji Shimizu, Hiromu Kawasaki, Toshiaki Sendo, Yutaka Gomita
Affiliations
Free article

Increased DOI-induced wet-dog shakes in adrenocorticotropic hormone-treated rats are not affected by chronic imipramine treatment: possible involvement of enhanced 5-HT(2A)-receptor expression in the frontal cortex

Yoshihisa Kitamura et al. J Pharmacol Sci. 2008 Jan.
Free article

Abstract

We examined the influence of imipramine, a traditional tricyclic antidepressant, on the binding to serotonin (5-HT)(2) receptors and levels of 5-HT(2A)-receptor mRNA in the frontal cortex of rats treated with adrenocorticotropic hormone (ACTH). Chronic treatment with ACTH significantly increased the binding of [(3)H]-ketanserin to 5-HT(2) receptors and the expression of 5-HT(2A)-receptor mRNA in the frontal cortex. However, it did not alter the concentration of 5-HT or 5-hydroxyindole acetic acid. The effect of chronic ACTH treatment on 5-HT(2) receptor and 5-HT(2A)-receptor mRNA levels was not altered by the chronic administration of imipramine. Also, imipramine did not affect the hyperfunction of 5-HT(2A) receptors caused by chronic ACTH treatment. These findings suggest that chronic treatment with ACTH acts to increase 5-HT(2A)-receptor synthesis through increased gene transcription, without modulating presynaptic serotonergic neurotransmission.

PubMed Disclaimer

Publication types

MeSH terms