Horm Metab Res 2003; 35(9): 511-516
DOI: 10.1055/s-2003-42650
Original Basic
© Georg Thieme Verlag Stuttgart · New York

Involvement of 5-HT2 Receptor in Imipramine-Induced Hyperglycemia in Mice

Y.  Sugimoto1 , K.  Inoue1 , J.  Yamada1
  • 1Department of Pharmacology, Kobe Pharmaceutical University, Motoyamakita-machi, Higashinada-ku, Kobe, Japan
Further Information

Publication History

Received 30 December 2002

Accepted after Revision 14 April 2003

Publication Date:
30 September 2003 (online)

Abstract

Effects of imipramine on plasma glucose levels were investigated in mice. Imipramine i. p. induced dose-dependent hyperglycemia, which was enhanced by pretreatment with 5-HT1/2/5/7 receptor antagonist methysergide and 5-HT2A/2B/2C receptor antagonist LY 53 857. 5-HT2C/2B receptor antagonist SB 206 553 also augmented imipramine-induced hyperglycemia although 5-HT1A and 5-HT1B receptor antagonist (-)-propranolol,5-HT2A receptor antagonist ketanserin and 5-HT3/4 receptor antagonist tropisetron each had no effect. Imipramine i. p.-induced hyperglycemia was antagonized by the 5-HT2C/2B receptor agonist 1-(3-chlorophenyl)piperazine (mCPP), while the 5-HT2B receptor agonist BW 723C86 had no effect. Intracerebroventricular injection of imipramine also elevated plasma glucose levels, which is enhanced by SB 206 553. Hyperglycemia elicited by central injection of imipramine was abolished by adrenalectomy. These results suggest that imipramine-induced hyperglycemia in mice is related to its inhibition of the central 5-HT2C receptor. Moreover, our results indicate that adrenaline release is related to imipramine-induced hyperglycemia.

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Y. Sugimoto

Department of Pharmacology · Kobe Pharmaceutical University

Motoyamakita-machi · Higashinada-ku · Kobe 658-8558 · Japan

Phone: +81(78)441-7573

Fax: +81(78)441-7574 ·

Email: yumisugi@kobepharma-u.ac.jp

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