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1982年Schafer和Jones根据肝性脑病(HE)时血γ-氨基丁酸(GABA)浓度、血脑屏障(BBB)及脑GABA受体等改变特征,在HE发病机制方面提出了GABA与HE有关的假设。 GABA的代谢与生理特征中枢神经系统GABA系谷氨酸经谷氨酸脱浚酶催化脱羧而生成。外周组织合成GABA则通过另一途径,即脑内GABA是脊椎动物大脑的主要抑制性神经递质,比多巴胺、去甲肾上腺素、乙酰胆碱、血清素等生物胺神经递质浓度高出200～1,000倍,绝大多数存在于突触前神经原中的贮存囊泡内而无生物效应。仅当突触前神经原
1982 Schafer and Jones based on changes in the concentration of GABA, BBB and brain GABA receptors in hepatic encephalopathy (HE), GABA and HE in the pathogenesis of HE was proposed Assumptions. GABA metabolic and physiological characteristics of the central nervous system GABA Department of glutamate by glutamate enzyme catalyzed decarboxylation generated. The synthesis of GABA by peripheral tissues is another way, that brain GABA is the main inhibitory neurotransmitter in vertebrate brain, higher than the concentration of biogenic amine neurotransmitters such as dopamine, norepinephrine, acetylcholine, serotonin 200 to 1,000 Times, the vast majority exist in the pre-synaptic neuron storage vesicles without biological effects. Only when presynaptic neurons