The effect of gamma-aminobutyric acid (GABA) on intracellular pH (pHi) was examined in the crayfish stretch-receptor neurone using H(+)-selective microelectrodes and a two-microelectrode voltage clamp. In the presence of 30 mmol l-1 HCO3- (pH 7.4), application of GABA (0.5 mmol l-1) produced a mean fall in pHi of 0.26 units. The initial rate of fall of pHi was attributable to a net influx of acid equivalents of 6.3 mmol l-1 min-1. In the nominal absence of HCO3-, GABA had little effect on pHi. The HCO3(−)-dependent acidosis caused by GABA was inhibited by picrotoxin (0.1 mmol l-1) but not by depletion of extracellular and intracellular Cl-. Acetazolamide (0.1 mmol l-1) decreased the rate of fall of pHi caused by a step increase in CO2 partial pressure as well as by GABA, which indicates that the neurone contains carbonic anhydrase. In the presence of both Cl- and HCO3-, the reversal potential of the GABA-activated current was more positive than under nominally HCO3(−)-free conditions. In line with this, GABA induced a marked HCO3(−)-dependent depolarization, and this depolarizing action was enhanced in the absence of Cl- so as to lead to triggering of action potentials. All these observations support the conclusion that the GABA-induced fall in pHi is due to a net efflux of HCO3- through the inhibitory anion channels.
Studies on the Distribution of Factor I and Acetylcholine in Crustacean Peripheral Nerve