The specific effect of potassium on transmitter release by motor nerve terminals and its inhibition by calcium

Abstract

1. There exist two distinct effects of potassium on the transmitter release system, one which develops rapidly and another which becomes maximal much more slowly. The fast effect is inhibited by raised Ca(2+), which does not inhibit transmitter release evoked by depolarizing pulses. Thus the fast effect is not secondary to nerve terminal depolarization.2. The fast effect of K(+) was found to consist in an increase in the slope of the linear relation between log m.e.p.p. frequency and nerve terminal depolarization. This effect is complete within a few seconds, is inhibited by raised Ca(2+), and is not produced by prolonged focal or electrotonic depolarization, which instead tends to reduce the slope of log m.e.p.p. frequency vs. depolarization.3. A slope change effect like that of K(+) was not found with ouabain or ethanol, nor did these agents depress the slope change effect of K(+). The specific action of K(+) was not exerted on release evoked in the absence of Ca(2+) by ethanol, chloral hydrate, or raised osmotic pressure.4. It is suggested that the specific action of K(+) is to increase the lability of nerve terminal Ca permeability with respect to depolarization of the nerve terminal membrane, while the slow effect of K(+) simply reflects nerve terminal depolarization, slow to become maximal because of diffusion barriers limiting access of raised K(+) to the Ranvier nodes of motor axons.