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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >The 'peripheral-type' benzodiazepine (omega 3) receptor in hyperammonemic disorders.
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The 'peripheral-type' benzodiazepine (omega 3) receptor in hyperammonemic disorders.

机译：高氨血症患者中的“外周型”苯二氮卓（ω3）受体。

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Increased levels of brain ammonia occur in both congenital and acquired hyperammonemic syndromes including hepatic encephalopathy, fulminant hepatic failure, Reye's syndrome and congenital urea cycle disorders. In addition to its effect on neurotransmission and energy metabolism, ammonia modulates the expression of various genes including the astrocytic peripheral-type expression of the isoquinoline carboxamide binding protein (IBP), one of the components of the PTBR complex, is observed in brain and peripheral tissues following chronic liver failure as well as in cultured astrocytes exposed to ammonia. Increased densities of binding sites for the PTBR ligand [(3)H]-PK11195 are also observed in these conditions as well as in brains of animals with acute liver failure, congenital urea cycle disorders and in patients who died in hepatic coma. The precise role of PTBR in brain function has not yet fully elucidated, but among other functions, PTBR mediates the transport of cholesterol across the mitochondrial membrane and thus plays a key role in the biosynthesis of neurosteroids some of which modulate major neurotransmitter systems such as the gamma-aminobutyric acid (GABA(A)) and glutamate (N-methyl-D-aspartate (NMDA)) receptors. Activation of PTBR in chronic and acute hyperammonemia results in increased synthesis of neurosteroids which could lead to an imbalance between excitatory and inhibitory neurotransmission in the CNS. Preliminary reports suggest that positron emission tomography (PET) studies using [(11)C]-PK11195 may be useful for the assessment of the neurological consequences of chronic liver failure.
机译：先天性和后天性高氨血症综合征（包括肝性脑病，暴发性肝功能衰竭，里氏综合征和先天性尿素循环障碍）均会出现脑氨水平升高。除了对神经传递和能量代谢有影响外，氨还调节各种基因的表达，包括在大脑和周围环境中观察到异喹啉羧酰胺结合蛋白（IBP）（PTBR复合物的组成部分之一）的星形细胞外周型表达。慢性肝衰竭后的组织以及暴露于氨的培养星形胶质细胞。在这些情况下，以及在患有急性肝功能衰竭，先天性尿素循环紊乱的动物以及在肝昏迷中死亡的动物的大脑中，也发现了PTBR配体[（3）H] -PK11195的结合位点密度增加。 PTBR在脑功能中的确切作用尚未完全阐明，但在其他功能中，PTBR介导胆固醇跨线粒体膜的运输，因此在神经甾体的生物合成中起关键作用，其中一些激素可调节主要的神经递质系统，例如γ-氨基丁酸（GABA（A））和谷氨酸（N-甲基-D-天冬氨酸（NMDA））受体。 PTBR在慢性和急性高氨血症中的激活导致神经甾体合成的增加，这可能导致CNS中兴奋性和抑制性神经传递之间的失衡。初步报告表明，使用[（11）C] -PK11195的正电子发射断层扫描（PET）研究可能对评估慢性肝衰竭的神经系统后果有用。

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