Abstract
1. The purpose of the present study was to investigate the effects of verapamil, a Ca2+ channel blocker, on acetylcholine (ACh) release in the CNS. 2. Striatal slices of rats, prelabelled with [3H]-ACh, were superfused with Krebs'-Ringer solution. The slices were stimulated by electrical pulses (1 Hz) or by an excitatory amino acid, L-glutamate and the effects of verapamil on the release of ACh were examined. 3. Electrical stimulation produced an increase in [3H]-ACh release from the striatal slices. Exposure of the slices to verapamil significantly inhibited the stimulation-evoked [3H]-ACh release. 4. An endogenous excitatory amino acid, L-glutamate, also elicited the release of [3H]-ACh. Verapamil significantly reduced the L-glutamate-induced release of [3H]-ACh and the inhibitory effect of verapamil was more pronounced in the presence of Mg2+ in the medium. 5. The results of the present study demonstrate that verapamil inhibited both electrically- and chemically-stimulated [3H]-ACh release from the rat striatum. The inhibition of cholinergic transmission by verapamil might be related to the central effect of the Ca2+ channel blocker.
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