Molecular analysis of glutamatergic neurotransmission in hepatic encephalopathy (B05)

高氨降低神经胶质细胞共培养模型中AMPA受体（AMPAR）的神经元表达。然而，基础的突触能神经传递是以突触外AMPAR为代价完全维持的，而突触外AMPAR不再可用于突触增强。在这里，假设将被测试，是否限制突触可塑性的肝性脑病（HE）的动物模型，可能会导致认知功能障碍的临床HE，是由于突触外储备池的AMPAR减少。采用超分辨率显微镜和单粒子跟踪，我们将可视化AMPAR的条件下，高氨开发一个定量模型的突触后AMPAR贩运HE，从治疗策略可能会推导出。

High ammonia reduces neuronal expression of AMPA receptors (AMPARs) in a neuroglial co-culture model. Yet, basal glutamatergic neurotransmission is fully maintained at the expense of extrasynaptic AMPARs, which are no longer available for synaptic potentiation. Here, the hypothesis will be tested, whether the constraints of synaptic plasticity in animal models of hepatic encephalopathy (HE), that might cause the cognitive deficits in clinical HE, are due to a reduction in the extrasynaptic reserve pool of AMPARs. Employing superresolution microscopy and single particle tracking, we will visualize AMPARs under conditions of high ammonia to develop a quantitative model of postsynaptic AMPAR trafficking in HE, from which treatment strategies might be deduced.