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Vol. 285, Issue 3, 1219-1225, June 1998

Serotonergic Modulation of Acetylcholine Release from Cortex of Freely Moving Rats1

Maria Grazia Giovannini, Ilaria Ceccarelli, Beatrice Molinari, Marco Cecchi, Joseph Goldfarb and Patrizio Blandina

Dipartimento di Farmacologia Preclinica e Clinica (M.G.G., I.C., B.M., M.C., P.B.), Universitá di Firenze, 50134 Firenze, Italy and Department of Pharmacology, Mount Sinai School of Medicine CUNY (J.G), New York, New York

The modulation of acetylcholine (ACh) release by 5-HT3 receptor activation was studied using in vivo microdialysis. Spontaneous and K+-stimulated ACh release were measured in frontoparietal cortex and hippocampus of freely moving rats. Two consecutive exposures to high K+ produced ACh release of similar magnitude. In the cortex, serotonin (5-HT) failed to alter spontaneous ACh release, but caused a concentration-dependent decrease of K+-evoked ACh release. Phenylbiguanide (PBG) and m-chlorophenylbiguanide, two selective 5-HT3 agonists, mimicked the 5-HT responses, but 8-hydroxy-2-(di-n-propylamino)tetralin, a selective 5-HT1A agonist, was without effect. However, PBG failed to modify K+-evoked ACh release from the hippocampus. Systemic and local administration of a highly selective 5-HT3 antagonist, tropisetron ((3-alpha -tropanyl)1H-indole-carboxylic acid ester) blocked the effect of both 5-HT and PBG. The inhibition of ACh release by PBG was sensitive to tetrodotoxin. These observations provide direct evidence that, in rat cortex, 5-HT modulates in-vivo release of ACh through activation of 5-HT3 receptors.

0022-3565/98/2853-1219$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 1998 by The American Society for Pharmacology and Experimental Therapeutics


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