Kaila K, Voipio J
Department of Zoology, University of Helsinki, Finland.
Nature. 1987;330(6144):163-5. doi: 10.1038/330163a0.
Synaptic inhibition mediated by gamma-aminobutyric acid (GABA) is known to involve opening of receptor-gated chloride channels. Recent evidence indicates that these channels also show a significant permeability to the physiologically important bicarbonate anion. In all the excitable cells studied to date, the intracellular pH (pHi) is higher than would be predicted from a passive distribution of H+ ions, and consequently there is an outwardly directed electrochemical driving force for HCO3-. In the presence of CO2/HCO3- therefore, activation of GABA-gated channels could give rise to a significant efflux of bicarbonate, leading to a fall in postsynaptic pHi. We have examined the influence of GABA on pHi in crayfish skeletal muscle and we find that in the presence of CO2, GABA induces a dramatic fall in pHi which is coupled to an alkalosis at the extracellular surface. This fall in pHi and the extracellular alkalosis are attributable to a GABA-activated, picrotoxin-sensitive HCO3--conductance. In view of the sensitivity of ion channels and intracellular ion concentrations to changes in pHi, a GABA-induced postsynaptic acidosis could prove to be important in the modulation of inhibitory transmission.
已知由γ-氨基丁酸（GABA）介导的突触抑制涉及受体门控氯离子通道的开放。最近的证据表明，这些通道对生理上重要的碳酸氢根阴离子也具有显著的通透性。在迄今为止研究的所有可兴奋细胞中，细胞内pH值（pHi）高于根据H⁺离子被动分布所预测的值，因此存在针对HCO₃⁻的外向电化学驱动力。所以，在存在CO₂/HCO₃⁻的情况下，GABA门控通道的激活可能导致大量碳酸氢根外流，从而导致突触后pHi下降。我们研究了GABA对小龙虾骨骼肌pHi的影响，发现存在CO₂时，GABA会导致pHi急剧下降，这与细胞外表面的碱中毒相关。pHi的这种下降和细胞外碱中毒归因于GABA激活的、对印防己毒素敏感的HCO₃⁻电导。鉴于离子通道和细胞内离子浓度对pHi变化的敏感性，GABA诱导的突触后酸中毒可能在抑制性传递的调节中具有重要作用。
