Monoamines modulate the electrically-evoked efflux of 3H-choline from slices of guinea pig nucleus basalis magnocellularis.

The influence exerted by monoamines on acetylcholine release was studied in electrically stimulated slices of guinea pig nucleus basalis magnocellularis (nbM) prelabelled with 3H-choline (3H-Ch). Noradrenaline, 30 microM, and clonidine, 1 microM, reduced the evoked 3H-Ch efflux by about 50%, but phenylephrine, 100 microM, did not; idazoxan, 0.1 microM, but not prazosin, 1 microM, antagonized these effects, pointing to the involvement of alpha 2 receptors. Apomorphine, 1 or 30 microM, reduced 3H-Ch efflux from nbM slices as well. The effect was shared by quinpirole, 1 or 10 microM, but not by 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine (SKF 38393), 10 microM, and was antagonized by sulpiride, 1 microM, but not by R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepin++ +-7-ol (SCH 23390), 1 microM, suggesting the involvement of the D2 receptor subtype. 5-hydroxytryptamine (5-HT) 0.3-30 microM, and alpha-methyl-5-HT, 10 microM, significantly increased 3H-Ch efflux from nbM slices; the 5-HT2 antagonist ritanserin, 1 microM, prevented this response. 2-methyl-5-HT, 1-30 microM, inhibited the evoked 3H-Ch efflux and its effect was prevented by the 5-HT3 antagonist 1 alpha H,3 alpha,5 alpha H-tropan-3-yl-3,5-dichlorobenzoate (MDL 72222), 1 microM. These findings indicate that i) catecholamines inhibit nbM neurons through alpha 2 and D2 receptors and that ii) a complex serotonergic modulation of cholinergic function exists in the nbM, involving the activation of various receptor subtypes, which can mediate opposite responses.