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Endogenous GABAergic modulators in the pathogenesis of hepatic encephalopathy.

Abstract
Theories on the neurochemical etiology for hepatic encephalopathy have recently focussed on activation of inhibitory neurotransmitter GABA systems. Modulators of the GABAA receptor complex, including diazepam binding inhibitor, are significantly and selectively altered in hepatic encephalopathy. In animals and humans, benzodiazepine receptor antagonists rapidly ameliorate this syndrome suggesting the possible existence of an endogenous benzodiazepine-like substance. Endogenous GABAergic modulators may contribute to the neurochemical pathogenesis of hepatic encephalopathy.
AuthorsJ D Rothstein, M Olasmaa
JournalNeurochemical research (Neurochem Res) Vol. 15 Issue 2 Pg. 193-7 (Feb 1990) ISSN: 0364-3190 [Print] United States
PMID2159124 (Publication Type: Journal Article, Review)
Chemical References
  • Diazepam Binding Inhibitor
  • Neuropeptides
  • Receptors, GABA-A
  • Benzodiazepines
  • Flumazenil
Topics
  • Animals
  • Benzodiazepines (immunology, metabolism)
  • Diazepam Binding Inhibitor
  • Flumazenil (therapeutic use)
  • Hepatic Encephalopathy (drug therapy, metabolism, physiopathology)
  • Humans
  • Neuropeptides (metabolism)
  • Receptors, GABA-A (drug effects, metabolism)

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