Pathological role for exocytotic glutamate release from astrocytes in hepatic encephalopathy.
Pathological role for exocytotic glutamate release from astrocytes in hepatic encephalopathy.
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DOI：
10.2174/1570159x12666140903094700
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发表时间：
2014-07
影响因子：
5.3
通讯作者：
Parpura V
中科院分区：
文献类型：
--
作者：
Montana V;Verkhratsky A;Parpura V
肝衰竭可导致全身高氨血症，这被认为是肝性脑病的根本原因。这种神经精神综合征伴随着星形胶质细胞的功能变化。这些神经胶质细胞进入氨诱导的自我放大循环，其特征是脑水肿、氧化和渗透应激，导致蛋白质和 RNA 的修饰。因此，蛋白质表达和功能受到影响，包括谷氨酰胺合成酶和质膜谷氨酸转运蛋白的表达和功能，导致谷氨酸兴奋性毒性；星形胶质细胞的 Ca2+ 依赖性胞吐谷氨酸释放导致了这种细胞外谷氨酸超载。
Liver failure can lead to generalized hyperammonemia, which is thought to be the underlying cause of hepatic encephalopathy. This neuropsychiatric syndrome is accompanied by functional changes of astrocytes. These glial cells enter ammonia-induced self-amplifying cycle characterized by brain oedema, oxidative and osmotic stress that causes modification of proteins and RNA. Consequently, protein expression and function are affected, including that of glutamine synthetase and plasmalemmal glutamate transporters, leading to glutamate excitotoxicity; Ca2+-dependent exocytotic glutamate release from astrocytes contributes to this extracellular glutamate overload.