Dopamine release is enhanced while acetylcholine release is inhibited by nimodipine (Bay e 9736).
The calcium-channel ligand, nimodipine (Bay e 9736), in submicromolar concentrations (10(-7) to 10(-5) M), enhanced the potassium (25 mM) or electrical stimulation (1 Hz, 1 ms, 180 pulses) evoked release or [3H]dopamine from rat striatal slices, while it inhibited the release of [3H]acetylcholine. Nimodipine had similar effects on slices from the cerebral cortex loaded with [3H]dopamine or [3H]acetylcholine, the electrical stimulation evoked release of the catecholamine was enhanced, while release of [3H]acetylcholine was suppressed. The data indicate that nimodipine may distinguish between Ca2+ channels in dopaminergic and cholinergic nerve-terminals. The simultaneous elevation of dopamine release and suppression of acetylcholine release may prove useful in the treatment of Parkinson's disease.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism*; D004558:Electric Stimulation; D008297:Male; D009539:Nicotinic Acids / Q000494:pharmacology*; D009553:Nimodipine; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D002121:Calcium Channel Blockers; D009539:Nicotinic Acids; D009553:Nimodipine; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium; D004298:Dopamine