Kettenmann H
Can J Physiol Pharmacol. 1987 May;65(5):1033-7. doi: 10.1139/y87-163.
Cultured oligodendrocytes take up K+ triggered by an increase in [K+]o. Simultaneously [Cl-]i increases in the majority of the oligodendrocytes. This KCl uptake, which is not furosemide sensitive, can be explained by the following model. The first event is the entry of Cl- into the cell driven by the discrepancy between the membrane and Cl- equilibrium potential. As a consequence of the movement of negative charge across the membrane, K+ is driven into the cell. The prerequisites of this model, a passive Cl- distribution at resting membrane potential and a Cl- conductance of the membrane were found to exist in most cultured oligodendrocytes. The chloride equilibrium potential (-61 mV, SD +/- 10 mV) was slightly more positive than the membrane potential (-64 +/- 8 mV). Since cell input resistance determined with two independent electrodes increased by 11% (SD +/- 0.07) when [Cl-]o was reduced to 10 mM, part of the membrane conductance appears to be mediated by Cl-. Differences between membrane potential and Cl- equilibrium potential therefore will lead to Cl- fluxes across the membrane. In contrast with oligodendrocytes, [Cl-]i in astrocytes is significantly increased (from 20 to 40 mM) above the equilibrium distribution owing to the activity of an inward directed Cl- pump; this suggests a different mechanism of K+ uptake in these cells.
培养的少突胶质细胞会因细胞外钾离子浓度（[K⁺]o）升高而摄取钾离子。与此同时，大多数少突胶质细胞内的氯离子浓度（[Cl⁻]i）会升高。这种对呋塞米不敏感的氯化钾摄取现象可用以下模型解释。首先是氯离子因膜电位与氯离子平衡电位之间的差异而进入细胞。由于负电荷跨膜移动，钾离子被驱动进入细胞。已发现大多数培养的少突胶质细胞存在该模型的前提条件，即静息膜电位下氯离子的被动分布以及膜的氯离子电导。氯离子平衡电位（-61 mV，标准差±10 mV）略高于膜电位（-64±8 mV）。当细胞外氯离子浓度（[Cl⁻]o）降至10 mM时，用两个独立电极测定的细胞输入电阻增加了11%（标准差±0.07），这表明部分膜电导似乎由氯离子介导。因此，膜电位与氯离子平衡电位之间的差异将导致氯离子跨膜流动。与少突胶质细胞不同，由于内向氯离子泵的活动，星形胶质细胞内的氯离子浓度（[Cl⁻]i）比平衡分布时显著升高（从20 mM升至40 mM）；这表明这些细胞摄取钾离子的机制不同。
