Dual Effect of Potassium an Transmitter Release
Journal/Book: Reprinted from Nature Vol. 206 No. 4984 pp. 625-626 May 8 1965. 1965;
Abstract: Department of Physiology John Curtin School of Medical Research Australian National University Canberra A.C.T. *Post-doctoral Research Fellow Muscular Dystrophy Association of Canada The frequency of miniature end-plate potentials (m.e.p.p.s) is increased by passing depolarizing current through motor nerve terminals1 2. Raised extracellular concentrations of potassium ions also cause an increase in m.e.p.p. frequency and this effect has been attributed to depolarization of the nerve terminals2 3. However while depolarizing current reduces the amount of transmitter released by presynaptic nerve impulses4 raised potassium has the opposite effect3 5. This differente suggests that potassium ions may influence transmitter release by a mechanism distinct from depolarization of the nerve terminals. Such an action could well contribute to the increase of m.e.p.p. frequency caused by potassium. In support of this possibility it has occasionally been observed that the m.e.p.p. frequency in raised potassium continues to increase beyond the time when the ion would be expected to have reached its full concentration at the presynaptic nerve terminals6. The experiments described here were designed to investigate whether there is in fact a significant differente between the time taken by potassium to depolarize nerve terminals and the time for full development of the increase in m.e.p.p. frequency. . . .