King W M, Carpenter D O
Wadsworth Center for Laboratories and Research, New York State Department of Health, Albany 12201.
Neurosci Lett. 1987 Dec 4;82(3):343-8. doi: 10.1016/0304-3940(87)90280-1.
Using a microperfusion technique for rapid application of agonists to single identified voltage-clamped neurons of the marine mollusc Aplysia, chloride conductances elicited by gamma-aminobutyric acid (GABA) and L-glutamate were found to differ in rates of activation and desensitization, voltage dependence and dose-response relations. In spite of these marked differences, the two responses showed strong interaction: previous application of GABA could completely block the responses to glutamate while previous application of glutamate decreased the response to GABA. This interaction was not due to transmembrane chloride redistribution, and is probably not cross receptor blockade. Cross-desensitization of GABA and glutamate responses suggest that distinct receptors activate a common ion channel.
利用一种微灌流技术,将激动剂快速施加于海洋软体动物海兔单个经鉴定的电压钳制神经元上,结果发现,γ-氨基丁酸(GABA)和L-谷氨酸引发的氯电导在激活和脱敏速率、电压依赖性以及剂量反应关系方面存在差异。尽管存在这些显著差异,但这两种反应表现出强烈的相互作用:预先施加GABA可完全阻断对谷氨酸的反应,而预先施加谷氨酸则会降低对GABA的反应。这种相互作用并非由于跨膜氯再分布引起,而且可能也不是交叉受体阻断。GABA和谷氨酸反应的交叉脱敏表明,不同的受体激活了一个共同的离子通道。