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.
Imipramine - 5-HT (5-hydroxytryptamine, serotonin) - 5-HT2C/2B Receptor - Glucose - Antidepressants