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神经系统中的细胞外钾离子蓄积

Extracellular potassium accumulation in the nervous system.

作者信息

Orkand R K

出版信息

Fed Proc. 1980 Apr;39(5):1515-8.

PMID:7364046
Abstract

As a result of the normal electrical signaling of neurons, potassium accumulates in the narrow clefts separating the cellular elements of the nervous system. The increase in extracellular potassium, [K+]0 depends on the spatial and temporal pattern of electrical activity in the neurons and the removal of the accumulated K+ by diffusion, active transport, and current flow through cells. Increases in [K+]0 have been estimated indirectly by matching changes in nerve spikes and glial membrane potentials produced by activity with increases in [K+]0 bathing the preparation. Direct estimates have been made using K+-selective electrodes. Measurement with K+-selective electrodes and glial membrane potential have poorly defined spatial and temporal resolution; they indicate an "average" [K+]0 in the vicinity of the recording site. Under normal conditions elevated [K+]0 may modify the efficacy of synaptic transmission, vary rates of spontaneous spikes in neurons, increase sodium pumping in neurons, modify the sensitivity of receptors, and serve to coordinate neuronal activity with glial metabolism.

摘要

由于神经元正常的电信号传导,钾离子在分隔神经系统细胞成分的狭窄缝隙中积累。细胞外钾离子浓度[K+]0的增加取决于神经元电活动的时空模式以及通过扩散、主动转运和电流通过细胞来清除积累的钾离子。[K+]0的增加已通过将活动产生的神经尖峰和胶质细胞膜电位的变化与浸泡标本的[K+]0的增加相匹配来间接估计。已使用钾离子选择性电极进行直接估计。用钾离子选择性电极和胶质细胞膜电位进行测量时,其空间和时间分辨率定义不明确;它们指示记录部位附近的“平均”[K+]0。在正常情况下,升高的[K+]0可能会改变突触传递的效率,改变神经元自发尖峰的速率,增加神经元中的钠泵活动,改变受体的敏感性,并有助于协调神经元活动与胶质细胞代谢。

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