Endplate current fluctuations reveal only one channel type at frog neuromuscular junction

Abstract

SIGNAL transduction between nerve and muscle is mediated by a chemical process at the neuromuscular junction. In the nerve ending electrical activity causes the release of acetylcholine (ACh) into the synaptic cleft separating the nerve and muscle cells. ACh can bind to specific chemical receptors in the postjunctional muscle membrane; these receptors control a gating mechanism that can increase membrane conductance locally. Normal nervous activity triggers an action potential and contraction in twitch muscle fibres. At constant membrane potential the membrane conductance change induces a current that is carried largely by Na⁺ and K⁺ in frog¹, moving through ACh-gated membrane channels. There has been a controversy regarding the nature of the chemically gated endplate channels; are there kinetically-independent channels for Na⁺ and K⁺ , or are these ions transported by the same channel? Maeno² initially proposed separate endplate channels, arguing that the two component decay of endplate potentials in procaine-treated cells resulted from a selective effect on Na⁺ channel kinetics. Kordas^3,4 and Magleby and Stevens⁵ argued that Maeno's two-channel hypothesis could not account for the unique reversal potential observed or the monotonic voltage dependence of endplate current (EPC) decay. The analysis below of iontophoretically-induced EPC fluctuations in procaine-treated and untreated preparations indicates that the ions which constitute the EPC are not carried by kinetically distinguishable endplate channels.