The role of calcium in neuromuscular facilitation

Abstract

The hypothesis is put forward that a residue of the ''active Ca'' which enters the terminal axon membrane during the nerve impulse is responsible for short-term facilitation. This suggestion was tested on the myoneural junction by varying the local Ca concentration so that during the first of 2 nerve impulses [Ca]0 is either much lower than, or raised to a level approaching that, during the 2nd impulse. Facilitation is much larger in the latter case, which is in accordance with the ''Ca hypothesis''. A short pulse of depolarization focally applied to the junction is followed by a brief period of very intense facilitation. This can be seen in the tetordotoxin-treated preparation, e.g. by lengthening the depolarization from 1 to 2 msec. which can cause a more than 50-fold increase in transmitter release. This large ''early facilitation'' (which presumably occurs also during the course of a normal action potential) is discussed in relation to the ''Ca hypothesis''.