Inhibitory effects of verapamil on [3H]-acetylcholine release in the central nervous system of Sprague-Dawley rats.
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.
Tsuda
K
K
Neurochemistry Research Laboratories, New York University Medical Center, NY.
Tsuda
S
S
Goldstein
M
M
Masuyama
Y
Y
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002490:Central Nervous System / Q000187:drug effects / Q000378:metabolism*; D003864:Depression, Chemical; D004558:Electric Stimulation; D018698:Glutamic Acid / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D017072:Neostriatum / Q000187:drug effects / Q000378:metabolism; D009411:Nerve Endings / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D014700:Verapamil / Q000494:pharmacology*
D018698:Glutamic Acid; D014700:Verapamil; D000109:Acetylcholine