Szatkowski M, Schlue W R
Institut für Zoologie, Universität Düsseldorf, Germany.
Glia. 1992;5(3):193-200. doi: 10.1002/glia.440050305.
We used double-barrelled, neutral carrier, pH-sensitive microelectrodes to study the mechanisms by which the intracellular pH (pHi) is regulated in the connective glial cells of the medicinal leech. In HEPES-buffered, nominally CO2/HCO3(-)-free solutions the recovery of pHi from intracellular acidosis is Na(+)-dependent and reduced by at least half in the presence of amiloride, suggesting the action of Na+:H+ exchange. The rate of pHi recovery by this mechanism can be increased by raising the extracellular buffering power or by increasing extracellular pH. The presence of CO2/HCO3(-)-greatly increases the rate of pHi recovery from intracellular acidosis. This CO2/HCO3(-)-stimulated recovery is also dependent on external Na+, largely Cl(-)-independent, inhibited by DIDS, and accompanied by membrane hyperpolarization. This is consistent with it being mediated by the electrogenic cotransport of Na+ and HCO3- into the cells. A Cl(-)-dependent component to Na(+)- and HCO3(-)-dependent regulation is most easily explained by the added presence of a Na(+)-dependent exchange of HCO3- and Cl-.
我们使用双管、中性载体、pH敏感微电极来研究药用水蛭结缔组织神经胶质细胞中细胞内pH（pHi）的调节机制。在以HEPES缓冲、名义上不含CO2/HCO3(-)的溶液中，pHi从细胞内酸中毒状态的恢复依赖于Na(+)，并且在存在氨氯吡脒的情况下至少降低一半，这表明存在Na+:H+交换作用。通过提高细胞外缓冲能力或增加细胞外pH，可以提高这种机制导致的pHi恢复速率。CO2/HCO3(-)的存在极大地提高了pHi从细胞内酸中毒状态的恢复速率。这种由CO2/HCO3(-)刺激的恢复也依赖于细胞外Na(+)，很大程度上不依赖于Cl(-)，受DIDS抑制，并伴随着膜超极化。这与它由Na(+)和HCO3-的电生性协同转运进入细胞所介导是一致的。Na(+)和HCO3(-)依赖性调节中依赖于Cl(-)的成分最容易通过额外存在的Na(+)依赖性HCO3-和Cl-交换来解释。
