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皮质星形胶质细胞在低渗和等渗肿胀中牛磺酸外流的激活与失活:离子强度和细胞体积减小的作用

Activation and inactivation of taurine efflux in hyposmotic and isosmotic swelling in cortical astrocytes: role of ionic strength and cell volume decrease.

作者信息

Cardin V, Peña-Segura C, Pasantes-Morales H

机构信息

Institute of Cell Physiology, Department of Biophysics, National University of Mexico, Mexico City.

出版信息

J Neurosci Res. 1999 Jun 15;56(6):659-67. doi: 10.1002/(SICI)1097-4547(19990615)56:6<659::AID-JNR12>3.0.CO;2-W.

Abstract

A decrease in intracellular ionic strength appears involved in the activation of swelling-elicited 3H-taurine efflux in cortical cultured astrocytes. Hyposmotic (50%) or isosmotic urea-induced swelling leading to a decrease of intracellular ionic strength, activated 3H-taurine efflux from a rate constant of about 0.008 min(-1) to 0.33 min(-1) (hyposmotic) and 0.59 min(-1) (urea). This efflux rate was markedly lower (maximal 0.03 min(-1)) in isosmotic swelling caused by K+ accumulation, where there is no decrease in ionic strength, or in cold (10 degrees C) hyposmotic medium (maximal 0.18 min(-1)), where swelling is reduced and consequently intracellular ionic strength is less affected. Also, astrocytes pretreated with hyperosmotic medium, which recover cell volume by ion accumulation, did not release 3H-taurine when they swelled by switching to isosmotic medium, but when volume was recovered by accumulation of urea, taurine release was restored. These results point to a key role of ionic strength in the activation of osmosensitive 3H-taurine efflux. In contrast, its inactivation was independent of the change in ionic strength but appears related to the reduction in cell volume after swelling, since despite the extent or direction of the change in ionic strength, the 3H-taurine efflux did not inactivate in isosmotic KCl-elicited swelling when cell volume did not recover nor in hyposmotic swelling when RVD was impaired by replacing NaCl in the medium by permeant osmolytes.

摘要

细胞内离子强度的降低似乎参与了皮质培养星形胶质细胞中肿胀诱导的3H-牛磺酸外流的激活。低渗(50%)或等渗尿素诱导的肿胀导致细胞内离子强度降低,使3H-牛磺酸外流从约0.008 min(-1)的速率常数分别激活至0.33 min(-1)(低渗)和0.59 min(-1)(尿素)。在由K+积累引起的等渗肿胀(离子强度无降低)或冷(10℃)低渗培养基(肿胀减少,因此细胞内离子强度受影响较小,最大0.18 min(-1))中,这种外流速率明显较低(最大0.03 min(-1))。此外,用高渗培养基预处理的星形胶质细胞,通过离子积累恢复细胞体积,当切换到等渗培养基肿胀时不释放3H-牛磺酸,但当通过尿素积累恢复体积时,牛磺酸释放恢复。这些结果表明离子强度在激活渗透压敏感性3H-牛磺酸外流中起关键作用。相比之下,其失活与离子强度的变化无关,但似乎与肿胀后细胞体积的减少有关,因为尽管离子强度变化的程度或方向如何,在等渗KCl诱导的肿胀中当细胞体积未恢复时3H-牛磺酸外流不会失活,在低渗肿胀中当通过用渗透性溶质替代培养基中的NaCl损害调节性容积减小(RVD)时也不会失活。

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