Barker J L, Owen D G, Segal M
Neurosci Lett. 1984 Jun 29;47(3):313-8. doi: 10.1016/0304-3940(84)90532-9.
The membrane mechanisms associated with Cl- conductance activated by GABA in spinal and hippocampal neurons cultured from the embryonic mouse and rat have been studied with voltage- and patch-clamp techniques. The elementary mechanism underlying the conductance response is predominantly all-or-none with both similar and different kinetics in different assays. beta-Alanine and glycine also alter conductance via a similar mechanism, but the electrical properties associated with each transmitter are unique. Clinically important drugs modulate GABA-mediated responses by altering the kinetics of ion channel activity. Inhibitory synaptic currents whose time constant of decay coincides with the common, slower phase of channel kinetics in pharmacological experiments are altered in amplitude and/or time course by the same drugs. The results strongly suggest that the synaptic events reflect the activation of 1700 channels whose open-time distribution describes the time constant of decay.
利用电压钳和膜片钳技术，对从胚胎小鼠和大鼠培养的脊髓和海马神经元中由γ-氨基丁酸（GABA）激活的氯离子电导相关的膜机制进行了研究。电导反应的基本机制主要是全或无的，在不同实验中具有相似和不同的动力学。β-丙氨酸和甘氨酸也通过类似机制改变电导，但与每种递质相关的电学特性是独特的。临床上重要的药物通过改变离子通道活性的动力学来调节GABA介导的反应。在药理学实验中，其衰减时间常数与通道动力学常见的较慢相一致的抑制性突触电流，会被相同药物改变幅度和/或时间进程。结果强烈表明，突触事件反映了1700个通道的激活，其开放时间分布描述了衰减时间常数。
