The action of thallium acetate on neuromuscular transmission in the rat phrenic nerve-diaphragm preparation.
In the isolated phrenic nerve-hemidiaphragm preparation from the rat, thallium acetate induced a dose-dependent irreversible paralysis. There was a major time lag between the onset of the exposure and the decline in the indirectly elicited muscle twitches. The slope of the decline was in proportion to the applied concentration, which ranged from 1 X 10(-3) to 5 X 10(-6) mol/l. The paralysis was definitively manifest after approximately 40 min of incubation. In the phase of paralysis, both electrical stimulation of the muscle and chemical stimulation by addition of K+ were fully effective. However, addition of 4-aminopyridine and/or guanidine restored the indirect muscle twitches, indicating a previous reduction of synaptic activity by thallium. Lowering the Ca2+-concentration resulted in a reduced paralysis time. From these results it is suggested that thallium interferes with synaptic transmission by presynaptically antagonizing Ca2+-dependent processes.
D015761:4-Aminopyridine; D000631:Aminopyridines / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D003964:Diaphragm; D005260:Female; D019791:Guanidine; D006146:Guanidines / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009469:Neuromuscular Junction / Q000187:drug effects*; D009942:Organometallic Compounds; D010243:Paralysis / Q000139:chemically induced; D010791:Phrenic Nerve; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D009435:Synaptic Transmission / Q000187:drug effects*; D013793:Thallium / Q000494:pharmacology*
D000631:Aminopyridines; D006146:Guanidines; D009942:Organometallic Compounds; D013793:Thallium; D015761:4-Aminopyridine; D019791:Guanidine; C026995:thallium acetate; D011188:Potassium; D002118:Calcium