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丙戊酸(VPA)起初被用来治疗失神发作,近年来已经发展成为一广谱抗癫痫药(AED_(?))而广泛应用于临床。其抗癫痫机制仍在探索中,迄今为止的研究主要集中在三个方面:①增加脑部抑制性神经递质r-氨基丁酸(GABA)浓度;②加强突触后神经元对GABA的反应性;③推测VPA有直接的膜作用以降低神经元的兴奋性。 一、VPA增高脑组织GABA水平 Godln于1969年首先提出这一假说,并推测GABA的增加是GABA转氨酶(GABA-T)受抑制的结果,但
Valproic acid (VPA) was initially used to treat seizures and has been widely used clinically in recent years as a broad-spectrum antiepileptic drug (AED_ (?)). Its anti-epileptic mechanism is still being explored. So far the research has mainly focused on three aspects: ① increasing the concentration of brain-inhibitory neurotransmitter r-aminobutyric acid (GABA); ② enhancing the response of post-synaptic neurons to GABA ③ presumed VPA has a direct membrane effect to reduce the excitability of neurons. VPA increases brain tissue GABA levels Godln first proposed this hypothesis in 1969 and speculated that increased GABA is the result of the inhibition of GABA-T (GABA-T), but