EXCITOTOXICITY - EXPERIMENTAL CORRELATES TO HUMAN EPILEPSY
EXCITOTOXICITY - EXPERIMENTAL CORRELATES TO HUMAN EPILEPSY
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DOI：
10.1007/bf02816125
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发表时间：
1994-08-01
影响因子：
5.1
通讯作者：
HAMBERGER, A
中科院分区：
文献类型：
--
作者：
HAGLID, KG;WANG, S;HAMBERGER, A
对48例手术治疗的耐药性部分性癫痫患者的皮质活检进行神经化学观察，结果显示，与神经元特异性烯醇化酶相关的谷氨酸浓度增加了70-80%。其受体激动剂之一，红藻氨酸（KA），腹腔给药的大鼠，导致增加的边缘类型的癫痫活动的剂量依赖性的方式。KA注射还导致神经元细胞死亡和神经胶质增生，与癫痫发作活动的程度密切相关。在人类致痫皮质的活检中，神经元特异性烯醇化酶的浓度与胶质细胞酸性蛋白（星形胶质细胞的标志物）呈负相关，KA受体的刺激降低了神经丝最大亚基（NF-H）磷酸化的程度，这对结构稳定性和轴突运输有影响。磷酸化NF-H也在人类癫痫皮质中减少，表明兴奋性神经递质的过度活跃或轴突隔室的损失。
Neurochemical observations on cortical biopsies form 48 patients under surgical treatment for pharmacoresistant partial epilepsy showed a 70-80% increase in glutamate concentration when expressed in relation to neuron specific enolase. Intraperitoneal administration of one of its receptor agonists, kainic acid (KA), to the rat led to increased epileptogenic activity of the limbic type in a dose-dependent fashion. The KA injection also led to a neuronal cell death and a gliosis, closely correlated to the extent of seizure activity. In biopsies from human epileptogenic cortex, the concentration of neuron specific enolase correlated inversely to that of glial fibrillary acidic protein, a marker for astrocytic glial cells.Stimulation of the KA receptor decreased the extent of phosphorylation of the largest subunit of neurofilaments (NF-H) that have consequences for structural stability and axonal transport. Phosphorylated NF-H decreased also in human epileptic cortex, indicating either an overactivity of excitatory neurotransmitters or a loss of axonal compartments.