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Effects of long-term alpha-2 adrenergic antagonists and electroconvulsive treatments on the alpha-2 adrenoceptors modulating serotonin neurotransmission

R Mongeau, C de Montigny and P Blier

Department of Psychiatry, McGill University, Montreal, Quebec, Canada.

Previous results from our laboratory indicate that small doses of the alpha-2 adrenergic agonist clonidine increase serotonin (5-HT) neurotransmission by attenuating the release of endogenous norepinephrine (NE), as a result of the activation of alpha-2 adrenergic autoreceptors on NE neurons, and that high doses decrease 5- HT neurotransmission by activating directly alpha-2 adrenergic heteroreceptors on 5-HT terminals. In addition, we have shown that long- term treatments with a monoamine oxidase inhibitor or a selective NE, but not a 5-HT, reuptake inhibitor abolish the effect of a high dose of clonidine, but not that of a small dose of clonidine. The aim of the present study was to determine whether the alpha-2 adrenergic antagonists idazoxan (10 mg/kg/day x 21 days s.c.) and mianserin (5 mg/kg/day x 21 days s.c.), or electroconvulsive shocks (6 or 7 over a 2- week period) would also affect the alpha-2 adrenoceptors modulating 5- HT neurotransmission in the rat hippocampus. The responsiveness of these hetereceptors was tested in parallel with those of the terminal 5- HT1B autoreceptors and of the postsynaptic 5-HT1A and alpha-2 adrenergic receptors. None of the above treatments altered the responsiveness of the 5-HT1B autoreceptors, as assessed by comparing the differential effectiveness of 1 and 5 Hz electrical stimulations of the 5-HT pathway. Idazoxan and mianserin did not affect the responsiveness of the postsynaptic 5-HT1A and alpha-2 adrenergic receptors as indicated by the unchanged suppressant effects of microiontophoretically applied 5-HT and NE.(ABSTRACT TRUNCATED AT 250 WORDS)

Volume 269, Issue 3, pp. 1152-1159, 06/01/1994
Copyright © 1994 by American Society for Pharmacology and Experimental Therapeutics




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