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在局灶性癫痫病灶部位,抑制性的γ-氨基丁酸能神经末梢数量减少。

Inhibitory, GABAergic nerve terminals decrease at sites of focal epilepsy.

作者信息

Ribak C E, Harris A B, Vaughn J E, Roberts E

出版信息

Science. 1979 Jul 13;205(4402):211-4. doi: 10.1126/science.109922.

Abstract

Using an immunocytochemical method for the localization of the gamma-aminobutyric acid (GABA) synthesizing enzyme, glutamic acid decarboxylase (GAD), we have observed GABAergic nerve terminals distributed throughout all layers of normal monkey sensorimotor cortex. These terminals displayed ultrastructural characteristics that suggested that they arose from aspinous and sparsely spinous stellate neurons. In monkeys (Macaca mulatta and M. fascicularis) made epileptic by cortical application of alumina gel, a highly significant numerical decrease of GAD-positive nerve terminals occurred at sites of seizure foci indicating a functional loss of GABAergic inhibitory synapses. A loss of such inhibition at seizure foci could lead to epileptic activity of cortical pyramidal neurons.

摘要

我们采用免疫细胞化学方法定位γ-氨基丁酸(GABA)合成酶——谷氨酸脱羧酶(GAD),观察到GABA能神经终末分布于正常猴感觉运动皮层的所有层。这些终末呈现出超微结构特征,提示它们起源于无棘和棘少的星状神经元。在通过皮层应用氧化铝凝胶而诱发癫痫的猴(恒河猴和食蟹猴)中,癫痫病灶部位的GAD阳性神经终末数量显著减少,表明GABA能抑制性突触功能丧失。癫痫病灶处这种抑制作用的丧失可能导致皮层锥体神经元的癫痫活动。

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