MONOAMINES MODULATE THE ELECTRICALLY-EVOKED EFFLUX OF H-3 CHOLINE FROM SLICES OF GUINEA-PIG NUCLEUS BASALIS MAGNOCELLULARIS

The influence exerted by monoamines on acetylcholine release was studi ed in electrically stimulated slices of guinea pig nucleus basalis mag nocellularis (nbM) prelabelled with H-3-choline (H-3-Ch) . Noradrenali ne, 30 mu M, and clonidine, 1 mu M, reduced the evoked H-3-Ch efflux b y about 50%, but phenylephrine, 100 mu M, did not; idazoxan, O.l mu M, but not prazosin, 1 mu M, antagonized these effects, pointing to the involvement of alpha(2) receptors. Apomorphine, 1 or 30 mu M, reduced H-3-Ch efflux from nbM slices as well. The effect was shared by quinpi role, 1 or 10 mu M, but not by tetrahydro-7,8-dihydroxy-1-phenyl-1H-3- benzazepine (SKF 38393), 10 uM, and was antagonized by sulpiride, 1 mu M, but not by (+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl- 1 H- 3-benzazepin-7-ol (SCH 23390), l mu M, suggesting the involvement of t he D-2 receptor subtype. 5-hydroxytryptamine (5-HT) 0.3-30 mu M, and a lpha-methyl-5-HT, 10 mu M, significantly increased H-3-Ch efflux from nbM slices; the 5-HT, antagonist ritanserin, 1 mu M,, prevented this r esponse. 2-methyl-5-HT, 1-30 mu M, inhibited the evoked H-3-Ch efflux and its effect was prevented by the 5-HT3 antagonist l alpha H,3 alpha ,5 alpha H-tropan-3-yl-3,5-dichlorobenzoate (MDL 72222), l mu M. These findings indicate that i) catecholamines inhibit nbM neurons through alpha, and D-2 receptors and that ii) a complex serotonergic modulatio n of cholinergic function exists in the nbM, involving the activation of various receptor subtypes, which can mediate opposite responses.