Raabe W, Lin S
Exp Neurol. 1985 Mar;87(3):519-32. doi: 10.1016/0014-4886(85)90181-5.
Ammonia intoxication affects postsynaptic inhibition and disturbs inhibitory neuronal interactions. This study investigated whether or not the effect of ammonia on postsynaptic inhibition was associated with a change of the EEG, i.e., a change in the function of the central nervous system such as in an encephalopathy. We showed that the effect of ammonia on postsynaptic inhibition was associated with a marked change of the EEG, and that this change was not due to an effect of ammonia on the brain stem reticular activating system. In addition, it was shown that in the central nervous system a NH+4 concentration of about 1 mumol/g affected postsynaptic inhibition. Because ammonia simultaneously affected postsynaptic inhibition and the EEG at a NH+4 tissue concentration comparable to that observed in encephalopathy, it is proposed that a dysfunction of postsynaptic inhibition caused the encephalopathy due to ammonia intoxication by simultaneously disturbing inhibitory neuronal interactions in many regions of the central nervous system.
氨中毒会影响突触后抑制并扰乱抑制性神经元相互作用。本研究调查了氨对突触后抑制的作用是否与脑电图(EEG)的变化相关,即是否与中枢神经系统功能的变化(如在脑病中)相关。我们发现氨对突触后抑制的作用与EEG的显著变化相关,且这种变化并非氨对脑干网状激活系统作用的结果。此外,研究表明在中枢神经系统中,约1微摩尔/克的NH₄⁺浓度会影响突触后抑制。由于在与脑病中观察到的组织NH₄⁺浓度相当的情况下,氨同时影响突触后抑制和EEG,因此有人提出突触后抑制功能障碍通过同时扰乱中枢神经系统许多区域的抑制性神经元相互作用,导致了氨中毒所致的脑病。