Rothstein J D, Olasmaa M
Johns Hopkins University, Department of Neurology, Baltimore, MD 21205.
Neurochem Res. 1990 Feb;15(2):193-7. doi: 10.1007/BF00972209.
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.