Synaptic plasticity at crayfish neuromuscular junctions: presynaptic inhibition.
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abstract
Intracellular recordings at sites electronically near terminals of the opener excitor axon in the claw of crayfish (Procambarus simulans) show that stimulation of the inhibitor neuron produces hyperpolarizing or depolarizing 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 50-70%. 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 short-term facilitation of excitatory transmitter release is not the same in all muscle fibers. In some terminals, the accumulation of short-term facilitation during short, high-frequency trains of action potentials which are presynaptically inhibited often equals the accumulation of facilitation without inhibition. In other terminals, short-term 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 short-term facilitation in some terminals.
