Coles J A, Orkand R K
J Physiol. 1983 Jul;340:157-74. doi: 10.1113/jphysiol.1983.sp014756.
Intracellular recordings were made in photoreceptors and glial cells (outer pigment cells) of the superfused cut head of the honey-bee drone (Apis mellifera male). When the [K+] in the superfusate was abruptly increased from 3.2 mM to 17.9 mM both photoreceptors and glial cells depolarized. The time course of the depolarization of the photoreceptors was slower with increasing depth from the surface. Half time of depolarization was plotted against depth: this graph was compatible with the arrival of K+ being exclusively by diffusion through the extracellular clefts. However, as we then showed, this interpretation is inadequate. The time course of depolarization of the glial cells was almost the same at all depths. This indicates that they are electrically coupled. Consequently, current-mediated K+ flux (spatial buffering) through glial cells will contribute to the transport of K+ through the tissue: K+ ions enter the glial syncytium in the region of high external potassium concentration, [K+]0, and an equivalent quantity of K+ ions leave in regions of low [K+]0. Intracellular K+ activity (aiK) was measured with double-barrelled K+-sensitive micro-electrodes in slices of retina superfused on both faces. When [K+] in the superfusate was increased from 7.5 mM to 17.9 mM an increase in aiK was observed in glial cells at all depths in the slice (initial rate 1.7 mM min-1, S.E. of the mean = 0.2 mM min-1), but there was little increase in the photoreceptors (0.3 +/- 0.2 mM min-1). The increase in aiK in glial cells near the centre of the slice could not have been caused by spatial buffering; it presumably resulted from net uptake. We conclude that when [K+] is increased at the surface of this tissue, the build up of K+ in the extracellular clefts depends on extracellular diffusion, spatial buffering and net uptake. The latter two processes, which have opposing effects, involve about 10 times as much K+ as the first. This is in rough agreement with less direct experiments on mammalian brain (Gardner-Medwin, 1977, 1983b).
在雄蜂（意大利蜜蜂）离体且有液体灌注的头部，对光感受器和神经胶质细胞（外部色素细胞）进行了细胞内记录。当灌注液中的[K⁺]从3.2 mM突然增加到17.9 mM时，光感受器和神经胶质细胞均发生去极化。光感受器的去极化时间进程随着离表面深度的增加而变慢。将去极化的半衰期与深度作图：该图符合K⁺仅通过细胞外间隙扩散到达的情况。然而，正如我们随后所表明的，这种解释并不充分。神经胶质细胞在所有深度的去极化时间进程几乎相同。这表明它们存在电耦合。因此，通过神经胶质细胞的电流介导的K⁺通量（空间缓冲）将有助于K⁺在组织中的转运：K⁺离子在细胞外钾浓度高（[K⁺]₀）的区域进入神经胶质细胞合体，等量的K⁺离子在[K⁺]₀低的区域离开。用双管K⁺敏感微电极测量了两面都有灌注的视网膜切片中细胞内K⁺活性（aiK）。当灌注液中的[K⁺]从7.5 mM增加到17.9 mM时，在切片所有深度的神经胶质细胞中均观察到aiK增加（初始速率为1.7 mM min⁻¹，平均标准误 = 0.2 mM min⁻¹），但在光感受器中几乎没有增加（0.3 ± 0.2 mM min⁻¹）。切片中心附近神经胶质细胞中aiK的增加不可能是由空间缓冲引起的；推测是由净摄取导致的。我们得出结论，当该组织表面的[K⁺]增加时，细胞外间隙中K⁺的积累取决于细胞外扩散、空间缓冲和净摄取。后两个过程具有相反的作用，涉及的K⁺量约为第一个过程的10倍。这与对哺乳动物脑进行的不太直接的实验大致相符（Gardner - Medwin，1977年，1983b）。
