[Non-quantal secretion of a mediator as factor determining consequences of acetylcholinesterase inhibition].
The mechanism of shortening MEPC decay phase after initial prolongation due to acetylcholinesterase inhibition by armine and neostigmine was studied by use of two-electrode voltage-clamp at the mice diaphragm Factors which switch off non-quantal secretion of acetylcholine from the nerve (acute denervation in vitro, ouabain, high concentration of magnesium ions) only slightly reduced the prolongation of MEPC caused by AChE inhibition. So, postsynaptic potentiation of MEPC by nonquantal ACh is not significant immediately after AChE inhibition. At the same time these factors abolished the process of shortening MEPC decay phase. It is concluded, that desensitization of the postsynaptic membrane induced by nonquantal ACh is the main mechanism of the MEPC shortening and that this mechanism can compensate insufficient AChE activity.
Giniatullin
R A
RA
Khazipov
R N
RN
Oranskaia
T I
TI
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001138:Armin / Q000494:pharmacology; D002800:Cholinesterase Inhibitors / Q000494:pharmacology*; D003714:Denervation; D003964:Diaphragm / Q000294:innervation; D004558:Electric Stimulation; D066298:In Vitro Techniques; D051379:Mice; D009388:Neostigmine / Q000494:pharmacology; D013569:Synapses / Q000502:physiology*; D013570:Synaptic Membranes / Q000502:physiology; D013997:Time Factors
D002800:Cholinesterase Inhibitors; D009388:Neostigmine; D001138:Armin; D000109:Acetylcholine
Nekvantovaia sekretsiia mediatora kak faktor, opredeliaiushchiĭ posledstviia ingibirovaniia atsetilkholinésterazy.