gamma-Aminobutyric acid (GABA) and hepatic encephalopathy: testing the validity of electroencephalographic evidence of the GABA hypothesis.
Some GABA-ergic drugs are known to produce electroencephalographic and behavioral signs of inhibition as well as alterations of the visual evoked potential (VEP) similar in shape and parameters to those in experimental fulminant hepatic failure. These findings, along with a number of biochemical findings, were considered to support the theory attributing hepatic encephalopathy to enhanced GABA-ergic transmission. The present review demonstrates that it is uncertain whether electrographic correlates of experimental encephalopathy can be attributed to faulty GABA-ergic mechanisms; nor it is clear whether drug-induced alterations of electrocortical potentials and those recorded in acute hepatic failure share a common pathogenesis. Special emphasis is put on findings with visual evoked potentials altered by drugs acting at GABA/benzodiazepine receptors to show the diversity of changes associated with the activity of the GABA system. Attention is called to the fact that brain GABA increase as a mechanism of hepatic encephalopathy was discussed without specifying the nature and anatomical location of allegedly impaired neural circuits utilizing the neurotransmitter.
D000818:Animals; D001519:Behavior / Q000502:physiology; D004569:Electroencephalography; D005074:Evoked Potentials, Visual; D006439:Hemodynamics; D006501:Hepatic Encephalopathy / Q000503:physiopathology*; D006801:Humans; D009435:Synaptic Transmission; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D005680:gamma-Aminobutyric Acid