Phillips I, Martin K F, Thompson K S, Heal D J
CNS Biology, Knoll Pharmaceuticals Research & Development, Nottingham NG1 1GF, UK.
Brain Res. 1998 Jul 6;798(1-2):330-2. doi: 10.1016/s0006-8993(98)00479-x.
The effect of gamma-aminobutyric acid (GABA) was investigated on cortical wedges prepared from male Sprague-Dawley rats. GABA evoked concentration-dependent depolarisations (EC50: 0.8 mM), which were attenuated by up to 60% when bicarbonate-buffered aCSF was replaced with HEPES-buffered aCSF. Responses to 1 mM GABA were attenuated by (-)-bicuculline and picrotoxin and were potentiated by chlordiazepoxide and pentobarbitone. Ionotropic glutamate receptor antagonists had no effect. We conclude that GABA-evoked depolarisations are mediated via GABAA receptors, arising in part from HCO3- efflux from cells.
研究了γ-氨基丁酸(GABA)对雄性斯普拉格-道利大鼠制备的皮质楔形组织的作用。GABA诱发浓度依赖性去极化(半数有效浓度:0.8 mM),当用HEPES缓冲的人工脑脊液替代碳酸氢盐缓冲的人工脑脊液时,这种去极化最多可减弱60%。对1 mM GABA的反应被荷包牡丹碱和印防己毒素减弱,并被氯氮卓和戊巴比妥增强。离子型谷氨酸受体拮抗剂无作用。我们得出结论,GABA诱发的去极化是通过GABAA受体介导的,部分源于细胞内HCO3-外流。