Inhibition of transmitter release in bullfrog sympathetic ganglia induced by gamma‐aminobutyric acid.

Abstract

Effects of GABA on the nicotinic synapses in bullfrog [R. catesbeiana] sympathetic ganglia were studied. When GABA (100 .mu.M-1 mM) was applied to the ganglion, the post-synaptic membrane depolarized slightly and transiently with a slight decrease in the membrane resistance. GABA (5 .mu.M-1 mM) decreased the amplitude of the fast excitatory post-synaptic potentials (fast EPSP) and its quantal content without a significant change in the quantal size, and these effects were seen even after the subsidence of the membrane depolarization. Picrotoxin (10 .mu.M) did not antagonize the GABA action. The sensitivity of the subsynaptic membrane to ACh was unaffected by GABA. The synaptic current underlying the fast EPSP was significantly depressed in the presence of GABA. Neither the frequency nor the amplitude of the miniature EPSP which occurred spontaneously were altered by GABA, in either normal or high K+ solutions. The depressant action of GABA on the fast EPSP was not changed in a high K+ solution, while it was markedly decreased in a Cl--deficient solution. A small, but significant reduction in the amplitude of the presynaptic terminal spike recorded with a focal extracellular electrode was observed under the effect of GABA. GABA inhibits synaptic transmission of bullfrog sympathetic ganglion mainly by decreasing the evoked release of transmitter and only partly by post-synaptic action. Possible mechanisms of the presynaptic action of GABA were discussed.