Dixon D B, Takahashi K, Bieda M, Copenhagen D R
Department of Ophthalmology, Beckman Vision Center, UCSF School of Medicine, San Francisco, CA 94143-0730, USA.
Vision Res. 1996 Dec;36(24):3925-31. doi: 10.1016/s0042-6989(96)00129-0.
Quinine increases the conductance of hemi-gap junctions in horizontal cells. We investigated the mechanisms of alkalinization and the hypothesis that quinine-induced alkalinization produced these conductance increases. We found that quinine-induced alkalinizations were not blocked by cobalt, amiloride, or DIDS. Therefore, this suggests that the alkalinization is not likely due to net proton flux through opened hemi-gap channels nor is it likely due to an action on Cl-/HCO3- exchanger or Na+/H+ exchanger, both of which are known to regulate pHi in the horizontal cells. Quinine increased hemi-gap conductance even when cells were recorded with patch pipets containing up to 80 mM HEPES. We conclude that quinine-induced alkalinization cannot account solely for the hemi-gap junctional conductance increases.
奎宁可增加水平细胞中半通道连接的电导。我们研究了碱化机制以及奎宁诱导的碱化导致这些电导增加的假说。我们发现，奎宁诱导的碱化不受钴、氨氯吡脒或二异丙基氟磷酸（DIDS）的阻断。因此，这表明碱化不太可能是由于质子通过开放的半通道的净通量所致，也不太可能是由于对Cl⁻/HCO₃⁻交换体或Na⁺/H⁺交换体的作用，这两种交换体均已知可调节水平细胞中的细胞内pH值。即使在用含有高达80 mM 4-(2-羟乙基)-1-哌嗪乙磺酸（HEPES）的膜片钳吸管记录细胞时，奎宁也会增加半通道电导。我们得出结论，奎宁诱导的碱化不能单独解释半通道连接电导的增加。
