The calcium channel activator, Bay K 8644, enhances K+-evoked efflux of acetylcholine and noradrenaline from rat brain slices.
Slices of rat brain were incubated with either (3H) choline (hippocampus) or (3H) noradrenaline (hypothalamus) and superfused with Krebs buffer. The release of (3H) acetylcholine and (3H) noradrenaline after inhibition of monoamine oxidase by pargyline was induced by a short exposure to Krebs buffer containing elevated K+ ions (25 mmol/l). Nifedipine (1 mumol/l) caused only a slight inhibition of noradrenaline efflux and was without effect on acetylcholine overflow. The calcium channel activator, Bay K 8644 (0.1-1 mumol/l), increased the K+-evoked efflux of both neurotransmitters. The additional efflux evoked by Bay K 8644 (0.3 mumol/l) was blocked by nifedipine (1 mumol/l). The results from the present study thus extend the earlier findings with the neurotransmitter 5-hydroxytryptamine to include noradrenaline and acetylcholine. The functional correlates for voltage operated calcium channels concerned with transmitter release are clearly a widespread phenomenon in the CNS.
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D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism*; D004357:Drug Synergism; D006624:Hippocampus / Q000378:metabolism; D007031:Hypothalamus / Q000378:metabolism; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects*; D008297:Male; D009543:Nifedipine / Q000031:analogs & derivatives* / Q000494:pharmacology; D009638:Norepinephrine / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains
D007473:Ion Channels; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009543:Nifedipine; D000109:Acetylcholine; D011188:Potassium; D009638:Norepinephrine