As it has been reported that depolarization-induced release of Ach is diminished by activation of presynaptic muscarinic-autoreceptor in rabbit hippocampus, the post-receptor mechanism of Ach release were investigated in this study.
The effect of oxotremorine, a well known synthetic muscarinic agonist, and N-ethylmaleimide (NEM) on electrically & K` (30 mM)-evoked release of 3H-acetylcholine in rabbit hippocampus were observed. In hippocampal slices, the responses to oxotremorine, a specific M2-receptor agonist, were characterized by decrement of Ach release, in a dose related fashion with doses ranging from 0.1 to 10 μM. NEM (30 μM) increased the Ach release and this effect was inhibited by oxotremorine. In synaptosomal preparations, 1011M oxotremorine decreased the Ach release which was induced by K+ (30 mM) & Caz+ (100 μM). NEM (30 μM) elicited the increments of basal & K+-evoked Ach release and the effects of oxotremorine were conipletly abolished by NEM pretreatment.
It was suggested from these results that the Gi-protein might play in the post-receptor mechanism of Ach release from rabbit hippocampus.
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