Sakai S, Tosaka T
Department of Physiology, Tokyo Medical University, Japan.
Neurochem Int. 1999 Mar;34(3):203-12. doi: 10.1016/s0197-0186(99)00004-2.
Hyposmolarity-induced taurine release was dependent on the decrease in medium osmolarity (5-50%) in the satellite glial cells of the bullfrog sympathetic ganglia. Release of GABA induced by hyposmolarity was much less than that of taurine. Omission of external Cl- replaced with gluconate totally suppressed taurine release, but only slightly suppressed GABA release. Bumetanide and furosemide, blockers of the Na+/K+/2Cl- cotransport system, inhibited taurine release by about 40%. Removal of external Na+ by replacement with choline, or omission of K+, suppressed taurine release by 40%. Antagonists of the Cl-/HCO3 exchange system, SITS, DIDS and niflumic acid, significantly reduced taurine release. The carbonic anhydrase inhibitor, acetazolamide, reduced the taurine release by 34%. Omission of external HCO3 by replacement with HEPES caused a 40% increase in the hyposmolarity-induced taurine release. Hyposmolarity-induced GABA release was not affected by bumetanide or SITS. Chloride channel blockers, 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and N-phenylanthranilic acid (DPC), practically abolished taurine release. Blockers of K+ channels, clofilium and quinidine, had no effect on the taurine release. The hyposmolarity-induced taurine release was considerably enhanced by a simultaneous increase in external K+. GABA was not mediated by the same transport pathway as that of taurine. These results indicate that Cl- channels may be responsible for the hyposmolarity-induced taurine release, and that Na+/K+/2Cl- cotransporter and Cl-/HCO3 exchanger may contribute to maintain the intracellular Cl- levels higher than those predicted for a passive thermodynamic distribution in the hyposmolarity-induced taurine release.
低渗诱导的牛磺酸释放取决于牛蛙交感神经节卫星神经胶质细胞培养基渗透压的降低（5-50%）。低渗诱导的GABA释放远少于牛磺酸。用葡萄糖酸盐替代外部Cl⁻完全抑制了牛磺酸释放，但仅轻微抑制了GABA释放。布美他尼和呋塞米，Na⁺/K⁺/2Cl⁻共转运系统的阻滞剂，抑制牛磺酸释放约40%。用胆碱替代外部Na⁺或去除K⁺，抑制牛磺酸释放40%。Cl⁻/HCO₃交换系统的拮抗剂，SITS、DIDS和氟尼辛，显著降低了牛磺酸释放。碳酸酐酶抑制剂乙酰唑胺使牛磺酸释放减少34%。用HEPES替代外部HCO₃导致低渗诱导的牛磺酸释放增加40%。低渗诱导的GABA释放不受布美他尼或SITS影响。氯离子通道阻滞剂，5-硝基-2-(3-苯丙基氨基)苯甲酸（NPPB）和N-苯基邻氨基苯甲酸（DPC），实际上消除了牛磺酸释放。K⁺通道阻滞剂，氯非铵和奎尼丁，对牛磺酸释放没有影响。外部K⁺同时增加可显著增强低渗诱导的牛磺酸释放。GABA与牛磺酸不是通过相同的转运途径介导的。这些结果表明，Cl⁻通道可能是低渗诱导牛磺酸释放的原因，并且Na⁺/K⁺/2Cl⁻共转运体和Cl⁻/HCO₃交换体可能有助于在低渗诱导的牛磺酸释放中维持细胞内Cl⁻水平高于被动热力学分布预测的水平。
