Aguilar M A, Miñarro J, Felipo V
Area de Psicobiología, Facultad de Psicología, Universitat de Valencia., Aptdo. 22109, Valencia, 46071, Spain.
Exp Neurol. 2000 Feb;161(2):704-13. doi: 10.1006/exnr.1999.7299.
The cerebral dysfunction associated with hepatic encephalopathy is generally considered to have hyperammonemia as one of its main causes. Hyperammonemia impairs the neuronal glutamate-nitric oxide-cyclic GMP pathway and the induction of NMDA receptor-dependent long-term potentiation in the hippocampus. We studied the performance of pre/neonatally and postnatally exposed rats to hyperammonemia on active avoidance, passive avoidance, and conditional discrimination tasks. Pre/neonatal hyperammonemia slowed learning of active avoidance behaviors and impaired memory for the passive avoidance task while postnatal hyperammonemia impaired learning on the conditional discrimination task. Hyperammonemia thus may produce cognitive disturbances that relate to the effects of ammonia on the neuronal glutamate-nitric oxide-cyclic GMP pathway.
与肝性脑病相关的脑功能障碍通常被认为其主要病因之一是高氨血症。高氨血症会损害神经元的谷氨酸-一氧化氮-环磷酸鸟苷途径以及海马体中依赖N-甲基-D-天冬氨酸（NMDA）受体的长时程增强效应的诱导。我们研究了产前/新生儿期和产后暴露于高氨血症的大鼠在主动回避、被动回避和条件辨别任务中的表现。产前/新生儿期高氨血症减缓了主动回避行为的学习，并损害了被动回避任务的记忆，而产后高氨血症则损害了条件辨别任务的学习。因此，高氨血症可能会产生与氨对神经元谷氨酸-一氧化氮-环磷酸鸟苷途径的影响相关的认知障碍。
