慢性癫痫中氨基酸诱导的离子电导的长期变化。

Long-term alterations in amino acid-induced ionic conductances in chronic epilepsy.

作者信息

Pumain R, Louvel J, Kurcewicz I

出版信息

Adv Exp Med Biol. 1986;203:439-47. doi: 10.1007/978-1-4684-7971-3_33.

Abstract

Extracellular free sodium (Na+)o and calcium (Ca2+)o concentration changes were measured in the rat motor cortex, using ion-selective microelectrodes. During ionophoretic applications of excitatory amino acids, decreases in (Na2+)o and in (Ca2+)o were observed. Ca2+ signals were not or very little modified by applications of tetrodotoxin while Na+ signals were slightly depressed, up to 20%. Laminar profile analysis revealed that, while the magnitude of Na+ signals was rather constant throughout the cortex, Ca2+ signals were largest in upper cortical layers. Lesioning and pharmacological experiments indicated that the corresponding permeabilities were most probably located on apical dendrites of pyramidal tract neurons. The relative amplitude of Na+ and Ca2+ signals induced by the release of the glutamate agonists N-methyl-D-aspartate, quisqualate and kainate and the shape of the laminar profile of such responses indicated that different ionic permeabilities located on different neurons underlie such responses. Similar experiments performed on chronic epileptogenic motor foci in rats indicated that the amino acid-induced ionic responses were altered. The significance of such alterations for epileptogenesis is discussed.

摘要

使用离子选择性微电极测量大鼠运动皮层细胞外游离钠（Na⁺）o和钙（Ca²⁺）o浓度变化。在离子电泳施加兴奋性氨基酸期间，观察到（Na²⁺）o和（Ca²⁺）o降低。应用河豚毒素时，Ca²⁺信号未被改变或改变很小，而Na⁺信号略有降低，高达20%。层流剖面分析显示，虽然整个皮层中Na⁺信号的幅度相当恒定，但Ca²⁺信号在皮层上层最大。损伤和药理学实验表明，相应的通透性很可能位于锥体束神经元的顶端树突上。由谷氨酸激动剂N-甲基-D-天冬氨酸、quisqualate和海人藻酸释放诱导的Na⁺和Ca²⁺信号的相对幅度以及此类反应的层流剖面形状表明，位于不同神经元上的不同离子通透性是此类反应的基础。对大鼠慢性致痫运动病灶进行的类似实验表明，氨基酸诱导的离子反应发生了改变。讨论了此类改变对癫痫发生的意义。