ACTIVATION OF GABA(B) RECEPTORS AT INDIVIDUAL RELEASING BOUTONS OF THE CRAYFISH OPENER NEUROMUSCULAR-JUNCTION PRODUCES PRESYNAPTIC INHIBITION

1. Presynaptic inhibition in crustaceans involves the activation of ga mma-aminobutyric acid-A (GABA(A)) receptors that produce an increase i n chloride conductance at excitatory axon terminals. Such inhibition p roduced by single inhibitory pulses is blocked by picrotoxin, a GABA(A ) antagonist. 2. Presynaptic inhibition produced by bath application o f GABA was not blocked by picrotoxin. Measurements of the membrane res istance of the excitatory axon terminals revealed that substantial pre synaptic inhibition still persisted after 50 mu M picrotoxin had compl etely blocked the increase in conductance produced by 10 mu M GABA. 3. Baclofen, a GABA(B) agonist, reduced release from the excitatory nerv e terminals, and 20H-Saclofen, a GABA(B) antagonist, blocked the effec t of baclofen and the presynaptic inhibition produced by 10 mu M GABA. 4. 20H-Saclofen alone did not block presynaptic inhibition produced b y 100 mu M GABA, and the combined action of both 20H-Saclofen and picr otoxin was required to block such effects. 5. The excitatory nerve ter minals seem to contain GABA(A) and GABA(B) receptors. The GABA(B) rece ptors are preferentially activated at lower GABA concentrations (in th e mu M range), whereas both the GABA(A) and GABA(B) receptors are acti vated at high GABA concentrations.