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苯二氮类药物(BZDs)可有效地对抗大部分动物实验性癫痫模型的癫痫发作,减少痫样放电的持续时间,并抑制其扩散。BZDs可提高许多全身给予惊厥剂动物的惊厥阈值,而且对由戊四氮、印防已毒素和比枯枯林碱诱发的痫样发作特别有效。对癫痫点燃发作模型和铝诱发的局灶性发作,以及一些遗传性癫痫动物模型,BZDs也有抗痫效果,这包括光敏性发作的狒狒、听源性发作的小白鼠和共济失调的小鼠变异体。BZDs选择性地引起变异动物的γ-氨基丁酸(GABA)能神经抑制性电位的增高。中枢神经系统中一种对BZDs高亲和力的结合位点已被确定,这种结合位点即BZD受体,是GABA_A受体氯离子通道复合体的一部分,它
Benzodiazepines (BZDs) are effective against seizures in experimental animal models of epilepsy in most animals, reducing the duration of epileptiform discharges and inhibiting their spread. BZDs raise the threshold of seizure in many systemic convulsant animals and are particularly effective in the detection of epileptic seizures induced by pentylenetetrazol, picrotoxin and nicotinamide. BZDs also have antiepileptic effects on epileptic-lighted seizures and aluminum-induced focal seizures, as well as in some animal models of hereditary epilepsy, including photo-induced baboons, auditory-onset white mice, and ataxia-prone mice Variants. BZDs selectively cause increased gamma-aminobutyric acid (GABA) neuroretinal potential in mutated animals. A high-affinity binding site for BZDs in the central nervous system has been identified. This binding site, the BZD receptor, is part of the GABA_A receptor chloride ion channel complex, which