Hösli L, Hösli E
Adv Biochem Psychopharmacol. 1983;37:35-46.
Autoradiographic binding studies have shown that 3H-GABA, 3H-glycine, their antagonists 3H-bicuculline and 3H-strychnine were bound to many neurones of cultured rat CNS. In contrast, glial cells did not reveal binding sites for any of the compounds studied. The electrophysiological studies showed that GABA and glycine caused a hyperpolarization of cultured spinal neurones. This hyperpolarization was accompanied by a decrease in membrane resistance which is probably due to an increased membrane permeability to Cl- and K+. On cultured glial cells, both GABA and glycine produced depolarizations which were, however, not associated with a change in membrane conductance. Measurements of the extracellular K+-concentration using ion-sensitive microelectrodes indicated that the glial depolarization was caused by an efflux of K+ from adjacent neurones. From our electrophysiological and autoradiographic studies it is suggested that unlike neurones, glial cells do not possess receptors for GABA and glycine.
放射自显影结合研究表明,³H - GABA、³H - 甘氨酸及其拮抗剂³H - 荷包牡丹碱和³H - 士的宁与培养的大鼠中枢神经系统的许多神经元结合。相比之下,胶质细胞未显示出对所研究的任何化合物的结合位点。电生理研究表明,GABA和甘氨酸可使培养的脊髓神经元超极化。这种超极化伴随着膜电阻的降低,这可能是由于膜对Cl⁻和K⁺的通透性增加所致。在培养的胶质细胞上,GABA和甘氨酸均产生去极化,但这与膜电导的变化无关。使用离子敏感微电极测量细胞外K⁺浓度表明,胶质细胞去极化是由相邻神经元的K⁺外流引起的。根据我们的电生理和放射自显影研究,提示与神经元不同,胶质细胞不具有GABA和甘氨酸的受体。