Pasantes-Morales H, Moran J, Schousboe A
Department of Neurosciences, National University of Mexico, Mexico City.
Glia. 1990;3(5):427-32. doi: 10.1002/glia.440030514.
Release of taurine in response to cell swelling induced by hyposmolarity was observed in cultured astrocytes. Efflux of 3H-taurine increased by 30% and 70% upon reductions in osmolarity of only 5% and 10%. Reductions in osmolarity of 20%, 30%, and 50% stimulated basal taurine release by 300%, 500%, and 1,500%, respectively. The properties of this volume-sensitive release of taurine were examined to investigate: 1) its association with K+ and Cl- fluxes, currently activated during volume regulation: 2) its relationship with Ca2(+)-dependent reactions; and 3) the mechanism of the taurine efflux process. Taurine release was unaffected by removal of Na+, Ca2+, or Cl-, by pimozide and trifluoperazine, or by agents disrupting the cytoskeleton. The K+ channel inhibitors barium, quinidine, tetraethylammonium, and gadolinium had no effect. Taurine release was reduced by furosemide, a blocker of K+/Cl- cotransport, but not by the more specific inhibitor, bumetanide. It was markedly reduced by the inhibitors of Cl- channels DIDS, SITS, and anthracene-9-carboxylate. Taurine efflux was pH-dependent, being reduced at low pH values. It was decreased at 4 degrees C but not at 14 degrees C or 20 degrees C. These results suggest that the volume-sensitive release of taurine is independent of K+ fluxes but may be associated with Cl- conductances. It also seems unrelated to Ca2(+)-dependent transduction mechanisms. The Na(+)-dependent taurine carrier apparently is not involved in the swelling-induced release process.
在培养的星形胶质细胞中观察到，低渗诱导的细胞肿胀会引发牛磺酸的释放。当渗透压仅降低5%和10%时，3H-牛磺酸的流出量分别增加了30%和70%。渗透压降低20%、30%和50%时，分别刺激基础牛磺酸释放增加300%、500%和1500%。对这种牛磺酸的容量敏感性释放特性进行了研究，以探讨：1）其与容量调节过程中当前激活的K+和Cl-通量的关联；2）其与Ca2(+)-依赖性反应的关系；3）牛磺酸流出过程的机制。去除Na+、Ca2+或Cl-、使用匹莫齐特和三氟拉嗪，或使用破坏细胞骨架的试剂，均不影响牛磺酸的释放。K+通道抑制剂钡、奎尼丁、四乙铵和钆没有作用。呋塞米（一种K+/Cl-共转运阻滞剂）可降低牛磺酸的释放，但更特异的抑制剂布美他尼则无此作用。Cl-通道抑制剂二异硫氰酸二苯乙烯磺酸钠（DIDS）、4,4'-二异硫氰酸芪-2,2'-二磺酸（SITS）和蒽-9-羧酸盐可显著降低牛磺酸的释放。牛磺酸流出依赖于pH，在低pH值时减少。在4℃时减少，但在14℃或20℃时不减少。这些结果表明，牛磺酸的容量敏感性释放与K+通量无关，但可能与Cl-电导有关。它似乎也与Ca2(+)-依赖性转导机制无关。Na(+)-依赖性牛磺酸载体显然不参与肿胀诱导的释放过程。
