首页> 外文期刊>Journal of Neuroscience Research >Activation and inactivation of taurine efflux in hyposmotic and isosmotic swelling in cortical astrocytes: role of ionic strength and cell volume decrease.
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Activation and inactivation of taurine efflux in hyposmotic and isosmotic swelling in cortical astrocytes: role of ionic strength and cell volume decrease.

机译:牛磺酸外排在皮质星形胶质细胞的低渗和等渗肿胀中的激活和失活:离子强度和细胞体积减少的作用。

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摘要

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.
机译:细胞内离子强度的降低似乎参与了皮质培养的星形胶质细胞中肿胀引起的3H-牛磺酸外流的激活。低渗(50%)或等渗尿素引起的肿胀导致细胞内离子强度降低,激活3H-牛磺酸外排的速率常数从约0.008 min(-1)到0.33 min(-1)(低渗)和0.59 min (-1)(尿素)。在由K +积累引起的等渗溶胀中,离子流没有显着降低;在冷(10摄氏度)的低渗介质中(最大0.18 min(-1)),这种流出速率明显较低(最大0.03 min(-1))。 ),肿胀减少,因此细胞内离子强度受到的影响较小。同样,用高渗介质预处理的星形胶质细胞通过离子积累来恢复细胞体积,当它们通过切换到等渗介质而膨胀时,不会释放3H-牛磺酸,但是当通过尿素积累而恢复体积时,牛磺酸的释放得以恢复。这些结果表明离子强度在渗透敏感性3H-牛磺酸外排的激活中起关键作用。相反,其失活与离子强度的变化无关,但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不同,但3H-牛磺酸的流出在等渗的KCl-中并未失活当细胞体积无法恢复时,可引起肿胀;当RVD通过用渗透性渗透液替代培养基中的NaCl而受损时,可引起低渗性肿胀。

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