Abstract
Intracellular recordings at sites electrotnically near terminals of the opener excitor axon in the claw of crayfish (Procambarus simulans) show that stimulation of the inhibitor neuron produces hyperpolarizing or depolarzing presynaptic inhibitory potentials (PIPs). GABA applied anywhere along the length of the opener excitor or inhibitor axons also produces hyperpolarizing or depolarizing potentials. The amplitude of action potentials (APs) at recording sites near some excitor terminals is reduced by an average of 6 mV during presynaptic inhibition, which also reduces excitatory postsynaptic Potentials (EPSPs) by 50β70%. The time course of AP reduction equals the time course of EPSP reduction and the amount of AP reduction is independent of the sign or amplitude of the PIPs. All these data are consistent with a hypothesis that a conductance increase produced by GABA in these presynaptic terminals of the excitor axon is responsible for presynaptic inhibition. However, the effect of presynaptic inhibition upon the accumulation of shortβterm facilitation of excitatory transmitter release is not the same in all muscle fibers. In some terminals, the accumulation of Shortβterm facilitation during shourt, highβfrequency trains of ction potentials which are presynaptically inhibited often equals the accumulation of facilitation without inhibition. In other terminals, shortβterm facilitation accumulated during presynaptic inhibition often does not equal facilitation accumulated in the absence of presynaptic inhibition. These data suggest that some other factor which may contribute to presynaptic inhibition, such as a direct effect to decrease calcium currents, may also affect shortβterm facilitation in some terminals.