Kettenmann H, Backus K H, Schachner M
Brain Res. 1987 Feb 24;404(1-2):1-9. doi: 10.1016/0006-8993(87)91349-7.
Cultured astrocytes from cerebral hemispheres of early postnatal rats responded to gamma-aminobutyric acid (GABA) with membrane depolarization. This depolarization was affected by changes in extracellular [Cl-] and depended on the membrane potential. The reversal potential of the GABA-induced depolarization was determined by double electrode voltage clamp or depolarization by elevated [K+]o and ranged between -38 and -53 mV. Cell input resistance decreased after addition of GABA with the same time course as the membrane depolarization. GABA responses were temperature dependent yielding a peak at about 14 degrees C. At higher temperatures a decrease in the GABA-induced depolarization was seen indicating that the depolarization may not be mediated by an enzyme-coupled carrier system. Addition of ouabain at different temperatures did not change the size of the GABA depolarization. This excludes the possibility that an electrogenic component of the temperature-sensitive Na+,K+-ATPase activity causes the decrease in GABA-dependent depolarization at higher temperatures. Intracellular [Cl-] was measured with Cl- sensitive microelectrodes and found to be higher than the value calculated for a free distribution according to the Nernst equation (-40 mV). Addition of furosemide did not alter the reversal potential, but reduced the size of the GABA-induced membrane depolarization. From these observations and previous experiments on the pharmacological properties of the membrane response we conclude that the ionic mechanism underlying the GABA-dependent membrane depolarization of astrocytes results from a transient increase in Cl- -conductance similar to that of the neuronal GABAA-receptor.
来自新生大鼠脑半球的培养星形胶质细胞对γ-氨基丁酸（GABA）产生膜去极化反应。这种去极化受细胞外[Cl⁻]变化的影响，并取决于膜电位。GABA诱导的去极化的反转电位通过双电极电压钳或升高[K⁺]ₒ诱导的去极化来确定，范围在-38至-53 mV之间。加入GABA后，细胞输入电阻随膜去极化的相同时间进程而降低。GABA反应具有温度依赖性，在约14℃时达到峰值。在较高温度下，GABA诱导的去极化减小，这表明该去极化可能不是由酶偶联载体系统介导的。在不同温度下加入哇巴因不会改变GABA去极化的大小。这排除了温度敏感的Na⁺,K⁺-ATP酶活性的电生成分导致较高温度下GABA依赖性去极化减小的可能性。用Cl⁻敏感微电极测量细胞内[Cl⁻]，发现其高于根据能斯特方程（-40 mV）计算的自由分布值。加入呋塞米不会改变反转电位，但会减小GABA诱导的膜去极化的大小。根据这些观察结果以及先前关于膜反应药理学特性的实验，我们得出结论，星形胶质细胞GABA依赖性膜去极化的离子机制是由Cl⁻电导的瞬时增加引起的，类似于神经元GABAA受体的情况。
