DO MOTOR‐NERVE TERMINALS HAVE γ‐AMINOBUTYRIC ACID RECEPTORS?

1 gamma-Aminobutyric acid (GABA, 0.1 to 1 mM) had no significant effect on the amplitude, rise time, half decay time or frequency of miniature endplate potentials (m.e.p.ps) at the frog or mouse neuromuscular junctions in vitro. 2 Addition of GABA (1 mM) to preparations previously treated with 11 mM K+-Ringer did not cause any further increase in m.e.pp. frequency. GABA also failed to increase the m.e.p.p. frequency in a low Cl--Ringer. 3 GABA (0.1 to 1 mM) did not reduce the high m.e.p.p. frequency induced by veratrine (20 to 40 mg/l). 4 GABA (0.5 to 1 mM) did not affect the amplitude of the extracellularly-recorded nerve terminal spike, whereas 15 mM [K+] reduced the spike. 5 The quantal content (m) of the evoked endplate potential was not significantly altered by GABA; 9 mM [K+] significantly increased m. 6 When external d.c. potential differences were recorded in a three-chambered bath, GABA (0.1 to 1 mM) produced a very small depolarization if applied to the phrenic nerve trunk, but not if applied to the pre-terminal axon/motor nerve terminal region. Carbachol (0.3 to 1 mM) evoked a small depolarization when applied to the nerve terminal chamber. 7 These results fail to provide evidence for the existence of GABA receptors on motor nerve terminals.