RELATIONS BETWEEN SLOW EXTRACELLULAR POTENTIAL CHANGES, GLIAL POTASSIUM BUFFERING, AND ELECTROLYTE AND CELLULAR-VOLUME CHANGES DURING NEURONAL HYPERACTIVITY IN CAT BRAIN

RELATIONS BETWEEN SLOW EXTRACELLULAR POTENTIAL CHANGES, GLIAL POTASSIUM BUFFERING, AND ELECTROLYTE AND CELLULAR-VOLUME CHANGES DURING NEURONAL HYPERACTIVITY IN CAT BRAIN
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DOI:
10.1002/glia.440020104
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发表时间:
1989-01-01
期刊:
影响因子:
6.2
通讯作者:
LUX, HD
LUX, HD
中科院分区:
医学1区
文献类型:
--
作者:
DIETZEL, I;HEINEMANN, U;LUX, HD

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本研究的目的是估计空间胶质K+缓冲电流在增强神经元活动期间对细胞外K+稳态的贡献。电刺激猫皮层表面或丘脑腹基底核(5 ~ 50 Hz, 0.1 ~ 0.2 ms, 2 ~ 3倍阈值刺激强度,5 ~ 20 s)可诱导神经元亢进。在灰质上同时记录了8个相距300 μm的微移液管垂直组合的慢场电位变化。利用泊松方程,计算了潜在电流源和汇的幅值。电流源密度取决于记录深度、频率、强度和刺激持续时间。电流吸收,相当于每升脑组织和细胞外空间中单价阳离子的0.1-0.5毫摩尔的去除,在皮层中层被观察到,而源则出现在表层和深层。这些汇和源可能代表K+通过空间缓冲电流在神经胶质膜上移动。用模型计算研究了这种程度的胶质缓冲电流的后果。结果表明,测量电解质和细胞外空间的体积变化(Dietzel et al.)。中华医学杂志,20 (3):432-439,1980;Exp. Brain Res. 46: 73-84, 1982)只能部分地用这种规模的空间缓冲电流来解释。计算值与神经元和神经胶质细胞内测量值的比较(Coles等)。安。中国生物医学工程学报,2006;Ballanyi等人。J. Physiol. 382: 159-174, 1987)表明空间缓冲结合了近似等摩尔的KCl转运,并且根据制备,还结合了K+/Na+在神经胶质膜上的交换。
The aim of this investigation is to estimate the contribution of spatial glial K+ buffer currents to extracellular K+ homeostasis during enhanced neuronal activity. Neuronal hyperactivity was induced by electrical stimulation of the cortical surface or the ventrobasal thalamic nuclei of cats (5–50 Hz, 0.1–0.2 ms, two to three times threshold stimulation intensity, 5–20 s). The accompanying slow field potential changes were recorded simultaneously across the grey matter with vertical assemblies of eight micropipettes glued 300 μm apart. Using the Poisson equation, the amplitudes of the underlying current sources and sinks were calculated. The current source densities depended on the depth of recording, frequency, strength, and duration of the stimulation. Current sinks, corresponding to a removal of 0.1–0.5 mmoles of monovalent cations per liter of brain tissue and second from the extracellular space, were observed in middle cortical layers, whereas sources appeared at superficial and deeper sites. These sinks and sources might represent K+ moved across glial membranes by spatial buffer currents. The consequences of glial buffer currents of this magnitude were investigated with model calculations. It turned out that measurements of electrolyte and volume changes of the extracellular space (Dietzel et al. Exp. Brain Res. 40: 432–439, 1980; Exp. Brain Res. 46: 73–84, 1982) could only partially be explained by spatial buffer currents of this magnitude. Comparison of the calculated values with intracellular measurements in neurons and glial cells (Coles et al. Ann. NY Acad. Sci. 481: 303–317, 1986; Ballanyi et al. J. Physiol. 382: 159–174, 1987) suggests that spatial buffering combines with an approximately equimolar KCl transport and, depending on the preparation, also K+/Na+-exchange across glial membranes.