Biogenic antagonists of the nicotinic receptor: their interactions with erabutoxin.
The hypothesis that the sensitivity of the nicotinic ACh-receptor is reduced by some neurotransmitters was evaluated by studying the interaction between these neurotransmitters and erabutoxin-b (ETX-b), known to bind irreversibly with the specific ACh-receptor site. It was found that the blocking action of ETX-b was apparently prevented by previous application of 5-HT, whereas it was not prevented by application of catecholamine (CA). These results indicate that 5-HT blocks the nicotinic ACh-receptor by interacting with the specific ACh binding site, whereas CA blocks it by interacting with an allosteric site of the ACh-receptor ionic channel complex.
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D002395:Catecholamines / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004546:Elapid Venoms / Q000494:pharmacology*; D004870:Erabutoxins / Q000494:pharmacology*; D007473:Ion Channels / Q000187:drug effects; D009045:Motor Endplate / Q000187:drug effects; D009132:Muscles / Q000294:innervation; D011898:Ranidae; D011950:Receptors, Cholinergic / Q000187:drug effects*; D011978:Receptors, Nicotinic / Q000187:drug effects*; D012701:Serotonin / Q000494:pharmacology*
D002395:Catecholamines; D004546:Elapid Venoms; D007473:Ion Channels; D011950:Receptors, Cholinergic; D011978:Receptors, Nicotinic; D012701:Serotonin; D004870:Erabutoxins; D000109:Acetylcholine