Neuromuscular defect after suppression of ion conductance.
In rat skeletal muscle, trimetazidine (TMZ) caused a transmission defect without directly blocking binding of acetylcholine--ionophore impairment. In vivo, TMZ produced low-amplitude and cumulative depression of successive muscle responses, and immediate posttetanic exhaustion. These features differed from the effects of alpha-bungarotoxin (alpha-BuTx) or immunization with acetylcholine receptor (experimental autoimmune myasthenia gravis [EAMG]). In vitro, TMZ-induced block was similar to both alpha-BuTx-induced block and EAMG in many respects, but there were differences in endplate potentials evoked during and after rapid repetitive activations. These differences suggest that antibodies to the acetylcholine receptor do not affect the ionophore.
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D002038:Bungarotoxins / Q000494:pharmacology; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D005260:Female; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009045:Motor Endplate / Q000187:drug effects; D009132:Muscles / Q000294:innervation; D009157:Myasthenia Gravis / Q000503:physiopathology; D009431:Neural Conduction / Q000187:drug effects*; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology*; D010791:Phrenic Nerve / Q000187:drug effects; D010879:Piperazines / Q000494:pharmacology*; D051381:Rats; D011950:Receptors, Cholinergic / Q000187:drug effects; D012584:Sciatic Nerve / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects; D014292:Trimetazidine / Q000494:pharmacology*; D014403:Tubocurarine / Q000494:pharmacology
D002038:Bungarotoxins; D007473:Ion Channels; D010879:Piperazines; D011950:Receptors, Cholinergic; D014292:Trimetazidine; D000109:Acetylcholine; D014403:Tubocurarine