Presynaptic effect of gamma-aminobutyric acid on the inhibitory nerve and nerve terminals in the crayfish neuromuscular junction.

Experiments were carried out in voltage-clamped fibres of the opener muscle of the first walking leg or claw of small crayfish. Repetitive discharges in the inhibitory nerve innervating the muscle were induced by adding serotonin (10(-6) mol/l) and forskolin (10(-4) mol/l) to the superfusate. Rates of nerve discharge were determined by recording nerve evoked inhibitory postsynaptic currents (IPSCs) in the voltage-clamped muscle fibre. Subsequently, the effect of gamma-aminobutyric acid (GABA) on the rate of IPSCs in normal and Cl- -deficient superfusate was investigated. In normal superfusate GABA (10(-5) mol/l) abolished the IPSCs whereas in Cl- -deficient superfusate GABA (10(-4) mol/l) enhanced the rate of IPSCs. Moreover, in Cl- -deficient superfusate the rate of asynchronous quantal release of inhibitory transmitter could be enhanced by GABA. The results indicate that in the crayfish neuromuscular junction the inhibitory axon is supplied with GABA receptors which may affect (a) axonal excitation and (b) quantal output at the inhibitory axon terminals.