Phasic secretion of acetylcholine at a mammalian neuromuscular junction.

Abstract

The transient increase in secretion of quanta of acetylcholine (phasic secretion) produced by an action potential or brief depolarizing current pulse in mouse phrenic nerve terminals was examined. Following an activating stimulus, there was a brief delay (minimum latency) followed by a sigmoidal increase in secretion which then decayed exponentially. The minimum latency, rise time and rate of decay of phasic secretion, whether elicited by action potentials or electrotonic depolarization, were all extremely sensitive to temperature, with Q10 as high as 4 at temperatures of 5-15.degree. C. Arrhenius plots of results showed a change in slope with temperature, the change appearing most marked at 20-25.degree. C. Phasic secretion in response to action potentials prolonged by inhibitors of K conductance (4-aminopyridine, uranyl, tetraethylammonium or Zn2+) showed an increase in minimum latency but no other change in time course. Depolarizing pulses of varying width (0.2-2 ms) applied to nerve terminals (in the presence of tetrodotoxin and 4-aminopyridine) affected minimum latency, but had no great effect on the time course of phasic secretion. Neither an increase in extracellular K+ concentration nor a decrease in pH had any effect on the time course of phasic secretion nor was any change produced by ethanol or octanol. Variations in extracellular Ca concentration, substitution of Sr2+ for Ca2+ and repetitive stimulation, while producing changes in the magnitude of secretion, produced no change in the time course of phasic secretion.