GABA enhances transmission at an excitatory glutamatergic synapse

GABA mediates both presynaptic and postsynaptic inhibition at many synapses . In contrast, we show that GABA enhances transmission at excitatory synaps es between the lateral gastric and medial gastric motor neurons and the gas tric mill 6a and 9 (gm6a, gm9) muscles and between the lateral pyloric moto r neuron and pyloric 1 (p1) muscles in the stomach of the lobster Homarus a mericanus. Two-electrode current-clamp or voltage-clamp techniques were use d to record from muscle fibers. The innervating nerves were stimulated to e voke excitatory junctional potentials (EJPs) or excitatory junctional curre nts. Bath application of GABA first decreased the amplitude of evoked EJPs in gm6a and gm9 muscles, but not the p1 muscle, by activating a postjunctio nal conductance increase that was blocked by picrotoxin. After longer GABA applications (5-15 min), the amplitudes of evoked EJPs increased in all thr ee muscles. This increase persisted in the presence of picrotoxin. beta-(Am inomethyl)-4-chlorobenzenepropanoic acid (baclofen) was an effective agonis t for the GABA-evoked enhancement but did not increase the postjunctional c onductance. Muscimol activated a rapid postsynaptic conductance but did not enhance the amplitude of the nerve-evoked EJPs. GABA had no effect on iont ophoretic responses to glutamate and decreased the coefficient of variation of nerve-evoked EJPs. In the presence or absence of tetrodotoxin, GABA inc reased the frequency but not the amplitude of miniature endplate potentials . These data suggest that GABA acts presynaptically via a GABA(B)-like rece ptor to increase the release of neurotransmitter.