Voipio J, Pasternack M, Rydqvist B, Kaila K
Department of Zoology, University of Helsinki, Finland.
J Exp Biol. 1991 Mar;156:349-60. doi: 10.1242/jeb.156.1.349.
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.
使用氢离子选择性微电极和双微电极电压钳，在小龙虾牵张感受器神经元中研究了γ-氨基丁酸（GABA）对细胞内pH值（pHi）的影响。在含有30 mmol l-1 HCO3-（pH 7.4）的情况下，施加GABA（0.5 mmol l-1）导致pHi平均下降0.26个单位。pHi下降的初始速率归因于酸当量以6.3 mmol l-1 min-1的净内流。在名义上不存在HCO3-的情况下，GABA对pHi几乎没有影响。GABA引起的依赖于HCO3-的酸中毒被苦味毒素（0.1 mmol l-1）抑制，但不受细胞外和细胞内Cl-耗竭的影响。乙酰唑胺（0.1 mmol l-1）降低了由CO2分压逐步升高以及由GABA引起的pHi下降速率，这表明该神经元含有碳酸酐酶。在同时存在Cl-和HCO3-的情况下，GABA激活电流的反转电位比在名义上无HCO3-条件下更正。与此一致的是，GABA诱导了明显的依赖于HCO3-的去极化，并且在不存在Cl-的情况下这种去极化作用增强，从而导致动作电位的触发。所有这些观察结果支持这样的结论，即GABA诱导的pHi下降是由于HCO3-通过抑制性阴离子通道的净外流所致。
