Torres M L, Ortega F, Cuaranta I, González J, Sanchez-Armass S
Departamento de Fisiología y Farmacología, Facultad de Medicina, Universidad Autónoma de San Luis Potosi, Av. V. Carranza 2405, San Luis Potosi, S.L.P., 78210, Mexico.
Neurochem Res. 2008 Aug;33(8):1574-81. doi: 10.1007/s11064-008-9685-x. Epub 2008 Apr 11.
The Na(+)/H(+) exchanger has been the only unequivocally demonstrated H(+)-transport mechanism in the synaptosomal preparation. We had previously suggested that a Cl(-)-H(+) symporter (in its acidifying mode) is involved in cytosolic pH regulation in the synaptosomal preparation. Supporting this suggestion, we now show that: (1) when synaptosomes are transferred from PSS to either gluconate or sulfate solutions, the Fura-2 ratio remains stable instead of increasing as it does in 50 mM K solution. This indicates that these anions do not promote a plasma membrane depolarization. (2) Based in the recovery rate from the cytosolic alkalinization, the anionic selectivity of the Cl(-)-H(+) symporter is NO(3)(-) > Br(-) > Cl(-) >> I(-) = isethionate = sulfate = methanesulfonate = gluconate. (3) PCMB 10 muM inhibits the gluconate-dependent alkalinization by 30 +/- 6%. (4) Neither Niflumic acid, 9AC, Bumetanide nor CCCP inhibits the recovery from the cytosolic alkalinization.
钠氢交换体一直是突触体标本中唯一明确证实的氢离子转运机制。我们之前曾提出,氯离子-氢离子同向转运体(在其酸化模式下)参与突触体标本中的胞质pH调节。作为这一观点的证据,我们现在表明:(1)当突触体从生理盐溶液转移到葡萄糖酸盐或硫酸盐溶液中时,Fura-2比率保持稳定,而不像在50 mM钾溶液中那样升高。这表明这些阴离子不会促进质膜去极化。(2)根据胞质碱化后的恢复率,氯离子-氢离子同向转运体的阴离子选择性为硝酸根>溴离子>氯离子>>碘离子=羟乙磺酸盐=硫酸盐=甲磺酸盐=葡萄糖酸盐。(3)10 μM对氯汞苯甲酸抑制葡萄糖酸盐依赖性碱化30±6%。(4)氟尼辛、9-蒽甲酸、布美他尼和羰基氰化物间氯苯腙均不抑制胞质碱化后的恢复。