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首页> 外文期刊>Glia >Glutamate Transporter-Associated Anion Channels Adjust Intracellular Chloride Concentrations during Glial Maturation
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Glutamate Transporter-Associated Anion Channels Adjust Intracellular Chloride Concentrations during Glial Maturation

机译：谷氨酸转运蛋白相关的阴离子通道在胶质效果期间调节细胞内氯化物浓度

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摘要

Astrocytic volume regulation and neurotransmitter uptake are critically dependent on the intracellular anion concentration, but little is known about the mechanisms controlling internal anion homeostasis in these cells. Here we used fluorescence lifetime imaging microscopy (FLIM) with the chloride-sensitive dye MQAE to measure intracellular chloride concentrations in murine Bergmann glial cells in acute cerebellar slices. We found Bergmann glial [Cl-](int) to be controlled by two opposing transport processes: chloride is actively accumulated by the Na+-K+-2Cl(-) cotransporter NKCC1, and chloride efflux through anion channels associated with excitatory amino acid transporters (EAATs) reduces [Cl-](int) to values that vary upon changes in expression levels or activity of these channels. EAATs transiently form anion-selective channels during glutamate transport, and thus represent a class of ligand-gated anion channels. Age-dependent upregulation of EAATs results in a developmental chloride switch from high internal chloride concentrations (51.6 +/- 2.2 mM, mean +/- 95% confidence interval) during early development to adult levels (35.3 +/- 0.3 mM). Simultaneous blockade of EAAT1/GLAST and EAAT2/GLT-1 increased [Cl-](int) in adult glia to neonatal values. Moreover, EAAT activation by synaptic stimulations rapidly decreased [Cl-](int). Other tested chloride channels or chloride transporters do not contribute to [Cl-](int) under our experimental conditions. Neither genetic removal of ClC-2 nor pharmacological block of K+-Cl- cotransporter change resting Bergmann glial [Cl-](int) in acute cerebellar slices. We conclude that EAAT anion channels play an important and unexpected role in adjusting glial intracellular anion concentration during maturation and in response to cerebellar activity.
机译：星形胶质体积调节和神经递质摄取均可致依赖于细胞内阴离子浓度，但是关于控制这些细胞中的内部阴离子稳态的机制很少。在这里，我们使用荧光寿命成像显微镜（FLIM）与氯化物敏感性染料MQAE测量急性小脑切片中鼠伯格曼胶质细胞的细胞内氯化物浓度。我们发现Bergmann Glial [Cl - ]（Int）由两个相反的运输过程控制：氯化物被Na + -K + -2Cl（ - ）Cotroansporter NKCC1积极积累，并通过与兴奋性氨基酸转运蛋白相关的阴离子通道进行氯化物渗透（ EAAT）将[CL - ]（INT）减少到不同于这些通道的表达水平或活动变化的值。在谷氨酸运输过程中瞬时形成阴离子选择性通道，因此代表一类配体门控阴离子通道。年龄依赖性上调eaats导致在早期发育期间从高内氯浓度（51.6 +/- 2.2mm，平均+/-为95％置信区间）的发育氯化物切换到成人水平（35.3 +/- 0.3mm）。同时阻塞EAAT1 / PLAST和EAAT2 / GLT-1在成人胶虫中增加了[CL - ]（INT）到新生儿价值。此外，突触刺激的EAAT激活迅速减少[Cl - ]（int）。其他测试的氯化物通道或氯化物转运蛋白在我们的实验条件下不会有助于[Cl - ]（Int）。既不遗传去除CLC-2也不是K + -Cl-Cotoransporter的药物块，急性小脑切片中的休息Bergmann胶质[Cl - ]（Int）。我们得出结论，EAAT阴离子通道在成熟期间调整胶质细胞内阴离子浓度和响应小脑活性时起着重要和意外的作用。

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