Interaction of the opiate antagonist, naltrexone methyl bromide, with the acetylcholine receptor system of the motor end-plate.
Naltrexone methyl bromide (NMB) caused alterations in both the amplitude and the time course of end-plate currents (EPC) recorded from rat muscle. The amplitudes were significantly lower than control, and the EPC decay was no longer singly exponential. There was also a decrease in the voltage dependence of the peak amplitude and the decay time constant of the EPCs. These findings suggest NMB is blocking the open state of the acetylcholine channel.
D000818:Animals; D005260:Female; D008564:Membrane Potentials / Q000187:drug effects; D009045:Motor Endplate / Q000187:drug effects*; D009270:Naloxone / Q000031:analogs & derivatives*; D009271:Naltrexone / Q000031:analogs & derivatives* / Q000494:pharmacology; D009469:Neuromuscular Junction / Q000187:drug effects*; D000644:Quaternary Ammonium Compounds; D051381:Rats; D011919:Rats, Inbred Strains; D011950:Receptors, Cholinergic / Q000187:drug effects*
D000644:Quaternary Ammonium Compounds; D011950:Receptors, Cholinergic; C032257:methylnaltrexone; D009270:Naloxone; D009271:Naltrexone