Lancaster B, Wheal H V
Neuroscience. 1984 May;12(1):267-75. doi: 10.1016/0306-4522(84)90152-0.
It has been suggested that the late hyperpolarisation following synaptic activation of hippocampal CA1 pyramidal neurons is activated by calcium influx. This hypothesis was examined using microelectrodes containing EGTA. Intracellular injection of EGTA blocked the afterhyperpolarisation which normally followed cell firing produced by injection of a depolarising current or the ionophoresis of glutamate onto the apical dendrites. In contrast, the hyperpolarisation following synaptic activation was resistant to EGTA. The results suggest that this potential is not dependent on intracellular Ca2+. Other possible mechanisms are discussed.
有人提出,海马CA1锥体神经元突触激活后的晚期超极化是由钙内流激活的。使用含有乙二醇双四乙酸(EGTA)的微电极对这一假设进行了检验。向细胞内注射EGTA可阻断通常在注入去极化电流或在顶端树突上离子导入谷氨酸后产生的动作电位后的超极化。相比之下,突触激活后的超极化对EGTA具有抗性。结果表明,这种电位不依赖于细胞内的钙离子。文中还讨论了其他可能的机制。