Pathophysiology of ammonia intoxication.
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.
D000085:Acetates / Q000506:poisoning*; D000200:Action Potentials; D000818:Animals; D002415:Cats; D002490:Central Nervous System / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000503:physiopathology; D003655:Decerebrate State; D004569:Electroencephalography; D005071:Evoked Potentials / Q000187:drug effects; D008564:Membrane Potentials; D009046:Motor Neurons / Q000502:physiology; D009433:Neural Inhibition / Q000187:drug effects; D009994:Osmolar Concentration; D013116:Spinal Cord / Q000503:physiopathology; D013569:Synapses / Q000187:drug effects
D000085:Acetates; C018824:ammonium acetate