Molecular mechanisms of K+ clearance and extracellular space shrinkage-Glia cells as the stars.,Glia

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Molecular mechanisms of K+ clearance and extracellular space shrinkage-Glia cells as the stars.
Glia ( IF 5.4 ) Pub Date : 2020-03-17 , DOI: 10.1002/glia.23824
Nanna MacAulay ₁

Affiliation

Neuronal signaling in the central nervous system (CNS) associates with release of K⁺ into the extracellular space resulting in transient increases in [K⁺]_o. This elevated K⁺ is swiftly removed, in part, via uptake by neighboring glia cells. This process occurs in parallel to the [K⁺]_o elevation and glia cells thus act as K⁺ sinks during the neuronal activity, while releasing it at the termination of the pulse. The molecular transport mechanisms governing this glial K⁺ absorption remain a point of debate. Passive distribution of K⁺ via Kir4.1‐mediated spatial buffering of K⁺ has become a favorite within the glial field, although evidence for a quantitatively significant contribution from this ion channel to K⁺ clearance from the extracellular space is sparse. The Na⁺/K⁺‐ATPase, but not the Na⁺/K⁺/Cl⁻ cotransporter, NKCC1, shapes the activity‐evoked K⁺ transient. The different isoform combinations of the Na⁺/K⁺‐ATPase expressed in glia cells and neurons display different kinetic characteristics and are thereby distinctly geared toward their temporal and quantitative contribution to K⁺ clearance. The glia cell swelling occurring with the K⁺ transient was long assumed to be directly associated with K⁺ uptake and/or AQP4, although accumulating evidence suggests that they are not. Rather, activation of bicarbonate‐ and lactate transporters appear to lead to glial cell swelling via the activity‐evoked alkaline transient, K⁺‐mediated glial depolarization, and metabolic demand. This review covers evidence, or lack thereof, accumulated over the last half century on the molecular mechanisms supporting activity‐evoked K⁺ and extracellular space dynamics.

中文翻译：

K+清除和细胞外空间收缩的分子机制——神经胶质细胞作为恒星。

中枢神经系统 (CNS) 中的神经元信号与 K ⁺释放到细胞外空间相关，导致 [K ⁺ ] _{o 的}瞬时增加。这种升高的 K ⁺被迅速去除，部分是通过相邻神经胶质细胞的摄取。这个过程与[K ⁺ ] _o升高并行发生，因此神经胶质细胞在神经元活动期间充当K ⁺汇，而在脉冲终止时释放它。控制这种胶质 K ⁺吸收的分子传输机制仍然是一个争论的焦点。K ⁺通过 Kir4.1 介导的 K ⁺空间缓冲被动分布已成为神经胶质领域的最爱，尽管这种离子通道对从细胞外空间清除K ⁺的定量显着贡献的证据很少。Na ⁺ /K ⁺ ‐ATPase，而不是 Na ⁺ /K ⁺ /Cl ^-协同转运蛋白 NKCC1，塑造了活性诱发的 K ⁺瞬态。在神经胶质细胞和神经元中表达的 Na ⁺ /K ⁺ -ATPase的不同同工型组合显示出不同的动力学特征，因此明显地针对它们对 K ^{+ 的}时间和数量贡献清除。长期以来，人们一直认为K ⁺瞬变引起的神经胶质细胞肿胀与 K ⁺摄取和/或 AQP4直接相关，尽管越来越多的证据表明它们并非如此。相反，碳酸氢盐和乳酸转运蛋白的激活似乎通过活性诱发的碱性瞬变、K ⁺介导的神经胶质去极化和代谢需求导致神经胶质细胞肿胀。这篇综述涵盖了过去半个世纪积累的关于支持活动诱发的 K ⁺和细胞外空间动力学的分子机制的证据或缺乏证据。

更新日期：2020-03-17

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