Raabe W
Exp Neurol. 1987 Jun;96(3):601-11. doi: 10.1016/0014-4886(87)90222-6.
Ammonia intoxication has been shown to decrease excitatory synaptic transmission in several regions of the central nervous system. To investigate the relation between an effect of ammonia on excitatory synaptic transmission and the behavioral depression in the encephalopathy due to ammonia intoxication, this study examined in the rat the effects of ammonia intoxication on the H-reflex, the behavioral and neurological signs of the encephalopathy due to ammonia intoxication, and correlated the effects on the H-reflex with the signs of encephalopathy. Ammonia intoxication abolished the H-reflex without affecting the M-response. This indicated that ammonia intoxication decreased spinal excitatory synaptic transmission without affecting neuromuscular excitatory synaptic transmission. In the encephalopathy due to ammonia intoxication, the H-reflex disappeared only during a very advanced stage of behavioral depression, i.e., coma. During early stages of behavioral depression, i.e., during a decrease of reactions to sensory stimuli, the H-reflex was not affected by ammonia intoxication. Therefore, mechanisms other than a decrease of excitatory synaptic transmission in the central nervous system may be responsible for the behavioral depression seen in early stages of the encephalopathy due to ammonia intoxication.
氨中毒已被证明会降低中枢神经系统多个区域的兴奋性突触传递。为了研究氨对兴奋性突触传递的影响与氨中毒性脑病中行为抑制之间的关系，本研究在大鼠中检测了氨中毒对H反射、氨中毒性脑病的行为和神经体征的影响，并将对H反射的影响与脑病体征进行了关联。氨中毒使H反射消失，而不影响M反应。这表明氨中毒降低了脊髓兴奋性突触传递，而不影响神经肌肉兴奋性突触传递。在氨中毒性脑病中，H反射仅在行为抑制的非常晚期阶段，即昏迷时消失。在行为抑制的早期阶段，即在对感觉刺激的反应降低期间，H反射不受氨中毒的影响。因此，中枢神经系统兴奋性突触传递降低以外的机制可能是氨中毒性脑病早期出现行为抑制的原因。
