Katzman R
Fed Proc. 1976 May 1;35(6):1244-7.
The development of potassium specific ion exchanger microelectrodes has enabled investigators to measure directly brain extracellular potassium ion activity. Although serum potassium in various species ranges between 3.5 and 6 mEq/l, brain extracellular potassium is maintained at a level close to 3 mEq/l independent of fluctuations in serum values. Despite this buffering of the internal brain environment by extracerebral changes, local variations in extracellular potassium occur in response to evoked neuronal activity, seizures, and spreading depression. Mechanisms involved in the maintenance of this ionic homeostasis in the brain include mediated transport at the level of the cerebral capillary and the choroid plexus epithelium. In addition, there are ouabain-sensitive clearance mechanisms presumably involving Na,K-ATPase that participate in the removal of excess potassium. The relative roles of simple diffusion, high glial cell conductance of potassium, and active ionic pumps in restoring basal potassium levels after activity are still controversial.
钾特异性离子交换微电极的发展使研究人员能够直接测量脑细胞外钾离子活性。尽管不同物种的血清钾浓度在3.5至6 mEq/l之间,但脑细胞外钾维持在接近3 mEq/l的水平,与血清值的波动无关。尽管脑外变化对脑内环境有这种缓冲作用,但细胞外钾的局部变化会因诱发的神经元活动、癫痫发作和扩散性抑制而发生。大脑中维持这种离子稳态的机制包括脑毛细血管和脉络丛上皮水平的介导转运。此外,存在可能涉及钠钾ATP酶的哇巴因敏感清除机制,参与去除多余的钾。在活动后恢复基础钾水平过程中,简单扩散、高钾胶质细胞电导率和活性离子泵的相对作用仍存在争议。