An endplate potential due to potassium released by the motor nerve impulse

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Abstract
A small endplate potential can be recorded in frog muscle fibers, after all acetylcholine-mediated transmission has been eliminated by pre- or postsynaptic blocking agents (botulinum toxin, Ca lack, Mn, curare, .alpha.-bungarotoxin). It is usually necessary to hyperpolarize the muscle membrane to detect this non-cholinergic endplate potential. Below -100 mV little or no response is seen; a maximum is reached at .apprx. -140 mV, when the amplitude can be as large as 100 .mu.V (endplate current up to .apprx. 1 nA). Other characteristic features are as follows: the response shows no quantal fluctuations; its amplitude is not facilitated by repetitive impulses; its size and time course are not noticeably affected by prostigmine, curare or .alpha.-bungarotoxin; the half-time of decline of the endplate current is .apprx. 1.7 ms at 20.degree. C, and is lengthened by lowering the temperature with a Q10 of .apprx. 1.3; the response is abolished by Ba. When iontophoretic pulses of K are applied to the endplate, local depolarization is recorded whose amplitude varies with membrane potential similarly to that of the nerve-evoked response. These observations strongly indicate that this non-cholinergic, non-quantal endplate potential arises from a rapid synaptic transfer of K ions, released by the active nerve terminal into the synaptic cleft and entering the muscle fiber through anomalous rectifier channels in the endplate membrane.