THE MODE OF OPERATION OF THE SYNAPTIC MECHANISM PRODUCING PRESYNAPTIC INHIBITION

Abstract

Several procedures were employed in investigating the synaptic mechanism that produces primary afferent depolarization (PAD) and so effects presynaptic inhibition. It was assumed that the synaptic transmitter acted on the primary afferent fibers in the same manner as transmitters at other synapses and causes a specific increase fa ionic permeability. The equilibrium potential probably is at a level of more than 30 mV depolarization relative to the resting membrane potential. The PAD recorded intracellularly from an afferent fiber has been subjected to the action of an impulse propagating down that fiber to its central terminals. The slow time course of the PAD is thus shown to be due to a transmitter action persisting for 100 to 200 msec. The spike potential of an afferent fiber was reduced when superimposed on a PAD fa that fiber, and this effect was increased when there was post-tetanic potentiation of the PAD. There was also a study of the effect of PAD in depressing monosynaptic EPSPs that were potentiated either during or after a tetanus.