Adaptation of the neuromuscular junction to chronic acetylcholinesterase inhibition due to phospholine treatment.
The disturbances of neuromuscular transmission due to chronic (1 to 30 days) administration of phospholine to rats were investigated upon the isolated diaphragm preparation. Phospholine treatment impaired the ability of the muscle to maintain tetanic contraction in response to indirect stimulation and caused post-tetanic depression of twitch responses. In the later stage marked recovery of neuromuscular function occurred in spite of further phospholine administration. This recovery was not accompanied by any increase in the already lowered acetylcholinesterase activity. The concentration of d-tubocurarine needed to block twitch response increased during the first days of phospholine treatment and then, during the following period gradually returned to the normal level. The concentration of carbachol needed to block twitch response during 2 to 30 days of continued treatment was higher than that in control animals. The possible explanations for the spontaneous recovery of neuromuscular function are discussed.
D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D002800:Cholinesterase Inhibitors; D003964:Diaphragm / Q000187:drug effects; D004456:Echothiophate Iodide / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects* / Q000201:enzymology; D051381:Rats; D013997:Time Factors; D014403:Tubocurarine / Q000494:pharmacology
D002800:Cholinesterase Inhibitors; D002217:Carbachol; D004456:Echothiophate Iodide; D014403:Tubocurarine