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癫痫的主要机制为脑内兴奋性氨基酸活性升高。在癫痫发作中,N-甲基-D-天门冬氨酸(NMDA)受体含量增多,表达升高,且其各个亚型之间相互作用,构形发生变化,使突触后膜支架蛋白磷酸化,发生级联发应,使NMDA受体配体离子通道持续开放,神经元持续放电,并向周围神经元放散扩布;长期癫痫反复发作,导致苔藓纤维发芽,神经元缺失;这些形态学和电生理改变,反之,导致癫痫的易感和反复发作。通过多年动物实验和临床应用,提示N-甲基-D-冬氨酸受体亚单位2B(NR2B),高选择性的拮抗剂有广阔的临床应用前景。
The main mechanism of epilepsy is brain excitatory amino acid activity increased. In epileptic seizures, N-methyl-D-aspartate (NMDA) receptor content increased, the expression increased, and its interaction between the various subtypes, configuration change, the postsynaptic scaffold protein Phosphorylation, cascade hair should occur, so that the NMDA receptor ligand ion channels continued to open, sustained discharge of neurons, and spread to peripheral neurons; long-term epileptic recurrent, leading to mossy fiber sprouting, neuronal loss; these morphologies Learning and electrophysiological changes, on the contrary, lead to epilepsy susceptibility and recurrent. Through years of animal experiments and clinical applications, it is suggested that N-methyl-D-aspartate receptor subunit 2B (NR2B) and highly selective antagonists have broad clinical application prospects.