Empson R M, Sheardown M J, Newberry N R
Cerebrus Ltd, Oakdene Court, 613 Reading Road, Winnersh, Berkshire, RG41 5UA, Wokingham, UK.
Eur J Pharmacol. 2000 Aug 11;401(3):339-42. doi: 10.1016/s0014-2999(00)00475-1.
Depolarising GABA(A) receptor-mediated responses recorded from the optic nerve using a grease gap technique were modulated by classical potentiators of GABA(A) receptors. The benzodiazepine, chlordiazepoxide, the barbiturate, pentobarbitone and the widely used anaesthetic, propofol, all potentiated gamma-aminobutyric acid (GABA) responses. They did so with different maximal efficacies, propofol>pentobarbitone>chlordiazepoxide, and potencies on the basis of EC(50) estimates, chlordiazepoxide>propofol>pentobarbitone. The greater than expected GABA potentiating properties of propofol were explained by a direct hyperpolarising action that occurred in the same concentration range as its action at the GABA(A) receptor but that was unlikely to be mediated by GABA(A) receptors.
使用油脂间隙技术从视神经记录的去极化GABA(A)受体介导的反应受到GABA(A)受体经典增强剂的调节。苯二氮䓬类药物氯氮卓、巴比妥类药物戊巴比妥以及广泛使用的麻醉剂丙泊酚,均增强了γ-氨基丁酸(GABA)反应。它们的最大效能不同,丙泊酚>戊巴比妥>氯氮卓,根据半数有效浓度(EC50)估计的效价,氯氮卓>丙泊酚>戊巴比妥。丙泊酚超出预期的GABA增强特性可通过直接超极化作用来解释,这种作用发生在与其作用于GABA(A)受体相同的浓度范围内,但不太可能由GABA(A)受体介导。