蛙视网膜扩散性抑制期间的 Müller 细胞功能
Müller cell function during spreading depression in frog retina.
作者信息
Mori S, Miller W H, Tomita T
出版信息
Proc Natl Acad Sci U S A. 1976 Apr;73(4):1351-4. doi: 10.1073/pnas.73.4.1351.
Abstract
K+ potentials were investigated using K+ microelectrodes in frog (Rana pipiens) retinas conditioned for spreading depression (SD) by Cl--free Ringer's solution. A marked increase in outside K+ concentration, [K+]O, maximal in the inner plexiform layer, was observed during SD. This [K+]o change resembled the simultaneously recorded membrane potential change in Müller cells, suggesting that these cells act as K+ electrodes. Intracellular recording with K+ electrodes in Müller cells showed that upon SD the [K+]i (inside) of Müller cells increases and therefore immediately starts to cleanse the extracellular space of the excess of K+ which, evidence suggests, is mainly caused by pathologically enhanced synaptic activity in the inner plexiform layer.
摘要
使用钾离子微电极在蛙（豹蛙）视网膜中研究钾离子电位，该视网膜用无氯林格氏液预处理以引发扩散性抑制（SD）。在扩散性抑制期间观察到细胞外钾离子浓度[K⁺]ₒ显著增加，在内网状层达到最大值。这种[K⁺]ₒ变化类似于同时记录的米勒细胞的膜电位变化，表明这些细胞起到钾离子电极的作用。用钾离子电极在米勒细胞内记录显示，在扩散性抑制时，米勒细胞的[K⁺]ᵢ（细胞内）增加，因此立即开始清除细胞外空间中过量的钾离子，有证据表明，这主要是由内网状层病理性增强的突触活动引起的。
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