Ammonia, postsynaptic inhibition and CNS-energy state.
Ammonia intoxication decreases the hyperpolarizing action of postsynaptic inhibition. This study examines the metabolic state of the spinal cord during this effect of ammonia intoxication on spinal motoneurons. ATP, ADP, AMP, the adenylate energy charge, glucose, PCr, pyruvate, alpha-ketoglutarate and glutamate were unchanged during the effect of ammonia on the hyperpolarizing action of postsynaptic inhibition. NH4+, glutamine and lactate were increased. Ammonia intoxication affected postsynaptic inhibition without changes of the resting membrane potential, the neuron input resistance, the action potential and EPSPs. The encephalopathy caused by ammonia intoxication is known to occur without an alteration of the tissue energy state. The effect of ammonia intoxication on postsynaptic inhibition can be considered as a cause of the encephalopathy because postsynaptic inhibition is altered without a change of the tissue energy state, the resting membrane potential, the whole neuron resistance, the action potential and EPSPs.
D000641:Ammonia / Q000494:pharmacology*; D000818:Animals; D001921:Brain / Q000378:metabolism; D001927:Brain Diseases / Q000139:chemically induced; D002415:Cats; D004734:Energy Metabolism / Q000187:drug effects*; D008564:Membrane Potentials / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects*; D009433:Neural Inhibition / Q000187:drug effects*; D013116:Spinal Cord / Q000187:drug effects*; D013268:Stimulation, Chemical; D009435:Synaptic Transmission / Q000187:drug effects
D000641:Ammonia