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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 astrocytic ('peripheral-type') benzodiazepine receptor: role in the pathogenesis of portal-systemic encephalopathy.
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The astrocytic ('peripheral-type') benzodiazepine receptor: role in the pathogenesis of portal-systemic encephalopathy.

机译：星形细胞（“外周型”）苯二氮卓受体：在门静脉系统性脑病的发病机理中的作用。

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摘要

An increasing body of evidence supports the notion that activation of astrocytic (peripheral-type) benzodiazepine receptors contributes to the pathogenesis of the central nervous system symptoms which are characteristic of portal-systemic encephalopathy (PSE). Binding site densities for the PTBR ligand [3H-PK11195] are increased in autopsied brain tissue from PSE patients as well as in the brains of animals with experimental chronic liver failure. In the case of the animal studies, increased PTBR sites resulted from increased PTBR gene expression. Exposure of cultured astrocytes to ammonia or manganese (two neurotoxic agents which under normal circumstances are removed by the hepatobiliary system and which are found to accumulate in brain in PSE) results in increased densities of [3H-PK11195] binding sites. Activation of PTBR is known to result in increased cholesterol uptake and increased synthesis in brain of neurosteroids some of which have potent positive allosteric modulator properties on the GABA-A receptor system. Accumulation of such substances in the brain in chronic liver failure could explain the neural inhibition characteristics of PSE.
机译：越来越多的证据支持这样一种观点，即星形细胞（外周型）苯二氮卓受体的激活有助于中枢神经系统症状的发病，而中枢神经系统症状是门静脉系统性脑病（PSE）的特征。 PTBR配体[3H-PK11195]的结合位点密度在PSE患者的尸体解剖脑组织以及实验性慢性肝衰竭动物的脑组织中均增加。在动物研究中，PTBR位点增加是由于PTBR基因表达增加所致。将培养的星形胶质细胞暴露于氨或锰（正常情况下会被肝胆系统清除的两种神经毒性剂，并发现它们会积聚在PSE的大脑中）导致[3H-PK11195]结合位点密度增加。已知PTBR的激活会导致神经甾体在胆固醇中的摄取增加和在大脑中的合成增加，其中一些神经固醇对GABA-A受体系统具有有效的正构构调节特性。慢性肝衰竭时大脑中此类物质的积累可以解释PSE的神经抑制特征。

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