The Journal of Neurophysiology Vol. 81 No. 3 March 1999, pp. 1184-1191
Copyright ©1999 by the American Physiological Society

Tonic Activation of Presynaptic GABA_B Receptors in the Opener Neuromuscular Junction of Crayfish

 ¹The Otto Loewi Minerva Center for Cellular and Molecular Neurobiology, Department of Neurobiology, The Hebrew University, Jerusalem, Israel; and  ²Department of Anaesthesia and Intensive Care, The University of Adelaide, Adelaide, South Australia 5005, Australia

Parnas, Itzchak, Grigory Rashkovan, Jennifer Ong, and David I. B. Kerr. Tonic activation of presynaptic GABA_B receptors in the opener neuromuscular junction of crayfish. 1184-1191 Release of excitatory transmitter from boutons on crayfish nerve terminals was inhibited by (R,S)-baclofen, an agonist at GABA_B receptors. Baclofen had no postsynaptic actions as it reduced quantal content without affecting quantal amplitude. The effect of baclofen increased with concentration producing 18% inhibition at 10 µM; EC₅₀, 50% inhibition at 30 µM; maximal inhibition, 85% at 100 µM and higher. There was no desensitization, even with 200 or 320 µM baclofen. Phaclofen, an antagonist at GABA_B receptors, competitively antagonized the inhibitory action of baclofen (K_D = 50 µM, equivalent to a pA₂ = 4.3 ± 0.1). Phaclofen on its own at concentrations below 200 µM had no effect on release, whereas at 200 µM phaclofen itself increased the control level of release by 60%, as did 2-hydroxy-saclofen (200 µM), another antagonist at GABA_B receptors. This increase was evidently due to antagonism of a persistent level of GABA in the synaptic cleft, since the effect was abolished by destruction of the presynaptic inhibitory fiber, using intra-axonal pronase. We conclude that presynaptic GABA_B receptors, with a pharmacological profile similar to that of mammalian GABA_B receptors, are involved in the control of transmitter release at the crayfish neuromuscular junction.