[3H]acetylcholine release from the phrenic nerve is increased or decreased by activation or desensitization of nicotine receptors.
Nicotinic agonists (nicotine, 1,1-dimethyl-4-phenylpiperazinium (DMPP) increased [3H]acetylcholine release when the pre-exposure time was short (20 s). This effect was antagonized by pretreatment with d-tubocurarine (d-TC), which indicates a receptor-mediated effect. After a longer pre-exposure time (3 min) 10 microM nicotine significantly decreased the evoked [3H]acetylcholine release, probably because desensitization of the nicotine autoreceptors had abolished the nicotinic autofacilitation of transmitter release.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D004246:Dimethylphenylpiperazinium Iodide / Q000494:pharmacology; D004594:Electrophysiology; D066298:In Vitro Techniques; D008297:Male; D009538:Nicotine / Q000378:metabolism; D010791:Phrenic Nerve / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000378:metabolism*
D011978:Receptors, Nicotinic; D004246:Dimethylphenylpiperazinium Iodide; D009538:Nicotine; D000109:Acetylcholine