ANALYSIS OF POTASSIUM DYNAMICS IN MAMMALIAN BRAIN-TISSUE
ANALYSIS OF POTASSIUM DYNAMICS IN MAMMALIAN BRAIN-TISSUE
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DOI：
10.1113/jphysiol.1983.sp014541
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发表时间：
1983-01-01
影响因子：
5.5
通讯作者：
GARDNERMEDWIN, AR
中科院分区：
文献类型：
--
作者：
GARDNERMEDWIN, AR
方程推导出K+动力学的简化模型的脑组织。这些描述了K+在细胞外空间中的运动，与通过细胞的电流相关的K+转移（所谓的空间缓冲机制）以及细胞外空间和细胞质之间的平衡。数值计算表明，从不同的实验室的K+动态的主要数据可以占空间缓冲作用和吸收的简单假设。许多数据与细胞外扩散是K+通过脑组织的主要机制不一致，包括一些早先引用的支持这一假设的数据。缓冲作用的空间缓冲传输的K+和细胞质的平衡，在这些机制中，减少上升[K +] o [胞外K+浓度]，否则会发生，定量分析特定的K+源分布和空间和时间的频率成分的一般干扰。空间缓冲作用在减少[K +] o升高方面具有最大的效果，在广泛的组织区域（> 0.0000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000000直径为200 μ m），持续大约几分钟的时间。可以实现> 75%的减少。随着局部但延长的释放，最大[K +] o升高几乎不受影响，但受更温和升高影响的组织体积大幅减少。细胞质K+吸收也有最大的影响与广泛的释放，但其影响随着释放时间的延长而减弱。缓冲机制和K+再摄取到活跃的神经元中确定的下降[K +] o一段时间的刺激后的影响被认为是。当再吸收的时间过程只有几秒钟时，再吸收不太可能是导致[K +] o下降的主要因素。介导的空间缓冲机制，可能是神经胶质细胞的细胞所必需的属性进行了评估。
Equations are derived for K+ dynamics in simplified models of brain tissue. These describe K+ movement in extracellular space, transfer of K+ associated with current flow through cells (the so-called spatial buffer mechanism) and equilibration between extracellular space and cytoplasm. Numerical calculations show that the principal data on K+ dynamics from various laboratories can be accounted for with simple assumptions about spatial buffer action and uptake. Much of the data is inconsistent with extracellular diffusion being the main mechanism for K+ flux through brain tissue, including some that was earlier cited in support of this hypothesis. The buffering actions of spatial buffer transfer of K+ and of cytoplasmic equilibration, in which these mechanisms reduce rises of [K+]o [extracellular K+ concentration] that would otherwise occur, are analyzed quantitatively for specific K+ source distributions and for spatial and temporal frequency components of general disturbances. Spatial buffer action has most effect in reducing [K+]o rises with net release over extensive zones of tissue (> .apprx. 200 .mu.m in diameter) for periods of the order of minutes. Reductions > 75% may be achieved. With localized but prolonged release, the maximum [K+]o rise is little affected but the volume of tissue affected by more moderate rises is substantially reduced. Cytoplasmic K+ uptake also has most effect with widespread release, but its effect diminishes with prolonged periods of release. The effects of the buffering mechanisms and of K+ re-uptake into active neurons in determining the decline of [K+]o after a period of stimulation are considered. Re-uptake is unlikely to be the major factor responsible for [K+]o decline when this has a time course of only a few seconds. The properties necessary for the cells mediating the spatial buffer mechanisms, possibly glial cells, are assessed.