Sawada M, Hara N, Ito I, Maeno T
J Neurosci Res. 1984;11(1):91-103. doi: 10.1002/jnr.490110110.
The ionic mechanism of a membrane effect of L-glutamate on two identified neurons in the buccal ganglion of Aplysia kurodai was investigated with conventional microelectrode techniques and glutamate iontophoresis. Bath-applied and iontophoresed glutamate hyperpolarized the membrane and increased the membrane conductance. The hyperpolarizing glutamate response decreased in amplitude and finally reversed its polarity by conditioning hyperpolarization. The reversal potential of the hyperpolarizing glutamate response was close to the ECl (-60 mV). The reversal potential changed by 22.4 mV when the external chloride concentration was altered by a factor of 5. The relationship between the iontophoretically applied current and the membrane conductance changes was suggestive of two glutamate molecules reacting with a single receptor site. The hyperpolarizing glutamate response was essentially unaffected by 2-amino-4-phosphonobutyric acid (2-APB), L-proline, and quinuclidinyl benzilate (QNB). It was concluded that the hyperpolarizing glutamate response was generated by an activation of Cl- conductance.
利用传统微电极技术和谷氨酸离子电泳法,研究了L-谷氨酸对黑背海兔口腔神经节中两个已鉴定神经元的膜效应的离子机制。浴用和离子电泳的谷氨酸使膜超极化并增加膜电导。通过条件性超极化,超极化谷氨酸反应的幅度减小,最终极性反转。超极化谷氨酸反应的反转电位接近氯离子平衡电位(-60mV)。当外部氯离子浓度改变5倍时,反转电位变化22.4mV。离子电泳施加的电流与膜电导变化之间的关系表明,两个谷氨酸分子与单个受体位点反应。超极化谷氨酸反应基本上不受2-氨基-4-膦酰丁酸(2-APB)、L-脯氨酸和东莨菪碱(QNB)的影响。得出的结论是,超极化谷氨酸反应是由氯离子电导的激活产生的。