Larsen Brian Roland, MacAulay Nanna
a Department of Cellular and Molecular Medicine; Faculty of Health and Medical Sciences ; University of Copenhagen ; Copenhagen , Denmark.
Channels (Austin). 2014;8(6):544-50. doi: 10.4161/19336950.2014.970448.
Neuronal activity results in release of K(+) into the extracellular space of the central nervous system. If the excess K(+) is allowed to accumulate, neuronal firing will be compromised by the ensuing neuronal membrane depolarization. The surrounding glial cells are involved in clearing K(+) from the extracellular space by molecular mechanism(s), the identity of which have been a matter of controversy for over half a century. Kir4.1-mediated spatial buffering of K(+) has been promoted as a major contributor to K(+) removal although its quantitative and temporal contribution has remained undefined. We discuss the biophysical and experimental challenges regarding determination of the contribution of Kir4.1 to extracellular K(+) management during neuronal activity. It is concluded that 1) the geometry of the experimental preparation is crucial for detection of Kir4.1-mediated spatial buffering and 2) Kir4.1 enacts spatial buffering of K(+) during but not after neuronal activity.
神经元活动导致钾离子（K⁺）释放到中枢神经系统的细胞外空间。如果允许过量的K⁺积累，随之而来的神经元膜去极化会损害神经元放电。周围的神经胶质细胞通过分子机制参与从细胞外空间清除K⁺，半个多世纪以来，其具体机制一直存在争议。Kir4.1介导的K⁺空间缓冲作用被认为是K⁺清除的主要贡献者，尽管其定量和时间贡献仍不明确。我们讨论了在确定Kir4.1在神经元活动期间对细胞外K⁺管理的贡献方面的生物物理和实验挑战。得出的结论是：1）实验准备的几何形状对于检测Kir4.1介导的空间缓冲至关重要；2）Kir4.1在神经元活动期间而非活动后发挥K⁺的空间缓冲作用。
