Hösli L, Hösli E, Andrès P F, Landolt H
Exp Brain Res. 1981;42(1):43-8. doi: 10.1007/BF00235727.
The action of inhibitory amino acid transmitters GABA, glycine, beta-alanine and taurine has been studied on the membrane potential of cultured astrocytes and on the extracellular K+-concentration ([K+]0) using K+-sensitive microelectrodes. All four amino acids caused a depolarization of glial cells and an increase of [K+]0. The effects produced by GABA were usually more pronounced than those caused by the other amino acids. Simultaneous recordings of the action of GABA and glycine on the glial membrane potential and on [K+]0 usually revealed a good correlation in time course, but often there were differences between the amplitudes of glial depolarizations and the values calculated from the [K+]0 increase. 4-Aminopyridine, which blocks K+-conductance of excitable membranes, reversibly abolished both the glial depolarization and the [K+]0 increased produced by GABA and glycine. From these results it is concluded that unlike neurones, glial cells do not have receptors for these amino acid transmitters and that their action on glial cells is caused by the efflux of K+ from activated neurones.
利用钾离子敏感微电极，研究了抑制性氨基酸递质γ-氨基丁酸（GABA）、甘氨酸、β-丙氨酸和牛磺酸对培养星形胶质细胞膜电位及细胞外钾离子浓度（[K⁺]₀）的作用。这四种氨基酸均引起神经胶质细胞去极化以及[K⁺]₀升高。GABA产生的效应通常比其他氨基酸引起的效应更明显。同时记录GABA和甘氨酸对神经胶质细胞膜电位及[K⁺]₀的作用，通常在时间进程上显示出良好的相关性，但神经胶质细胞去极化的幅度与由[K⁺]₀升高计算出的值之间常常存在差异。4-氨基吡啶可阻断可兴奋细胞膜的钾离子电导，它能可逆地消除GABA和甘氨酸所引起的神经胶质细胞去极化以及[K⁺]₀升高。从这些结果可以得出结论，与神经元不同，神经胶质细胞没有这些氨基酸递质的受体，并且它们对神经胶质细胞的作用是由活化神经元释放钾离子所引起的。
