Postsynaptic effects of ethanol at the frog neuromuscular junction.
The molecular mode of action of alcohol in the central nervous system (CN) is unclear. The effects of ethanol on axonal action potentials can only be measured at concentrations which are very much higher than those required to produce central effects. At the frog neuromuscular junction similar concentrations increase the open time (tau) of the ion channel associated with the nicotinic acetylcholine (ACh) receptor. We have now investigated the effect of ethanol on the postsynaptic membrane of the frog neuromuscular junction by measuring equilibrium dose-response curves for the interaction between the neuro-transmitter (ACh) and the ACh receptors. Using this system, we found that ethanol produces significant changes in receptor function. Moreover, we found that an ethanol concentration which can be physiologically tolerated by man (0.2%) the dose-response curve is measurably affected.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001001:Anura; D002217:Carbachol / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000494:pharmacology*; D066298:In Vitro Techniques; D007700:Kinetics; D009045:Motor Endplate / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects*; D011893:Rana esculenta; D011950:Receptors, Cholinergic / Q000187:drug effects*; D011978:Receptors, Nicotinic / Q000187:drug effects*
D011950:Receptors, Cholinergic; D011978:Receptors, Nicotinic; D000431:Ethanol; D002217:Carbachol; D000109:Acetylcholine