Transmitter amino acid neurochemistry in chronic alcoholism with and without cirrhosis of the liver

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Abstract
Neurotransmitter receptor studies are beginning to be applied more widely to human brain tissue obtained at autopsy. By taking tissue from well‐documented cases which have been extensively characterized on histological and morphometric criteria, it is becoming possible to make clinicopathological correlations in studies of the effects of chronic alcohol abuse. Recent findings of alterations in the nature and amounts of amino acid neurotransmitter receptors in alcoholism are summarized, with special emphasis on the effects of chronic severe liver disease. There are selective changes in receptors in the superior frontal cortex of alcoholics. There is a marked increase in the density of the GABA binding site, and a lesser change in the density of the ‘central‐type’ benzodiazepine site, on the GABAA‐benzodiazepine receptor complex. In contrast, glutamate receptors may be much less affected. Together with morphological and cognitive studies, the results suggest that the superior frontal cortex is preferentially damaged in chronic alcoholism. An increase in ‘central‐type’ benzodiazepine sites in both superior frontal cortex and motor cortex in cirrhotic alcoholics may reflect a more global brain damage, as observed in morphological studies. However, it should be noted the changes in [3H]GABA/muscimol binding were less pronounced in cirrhotic alcoholics than in non‐cirrhotic alcoholics.