Cerebral aminoacids in portal-systemic encephalopathy: lack of evidence for altered gamma-aminobutyric acid (GABA) function.
Construction of an end-to-side portocaval anastomosis in the rat resulted, 4 weeks later, in sustained hyperammonemia and two- to threefold increases in brain ammonia. Measurement of cerebral amino acids using a sensitive double-isotope dansyl microtechnique revealed substantial increases in the glutamine content of cerebral cortex and brain stem. Glutamate levels were found to be concomitantly reduced in both brain regions compared to those of sham-operated controls. The gamma-aminobutyric acid (GABA) content of cerebral cortex and brain stem was unaffected by portocaval shunting, as were activities of the GABA nerve-terminal marker enzyme glutamic acid decarboxylase (GAD). These findings suggest that impaired GABA function may not play a major role in the pathogenesis of hepatic encephalopathy associated with portocaval shunts. Preliminary evidence suggests that decreased cerebral glutamate may reflect its loss from the releasable (neurotransmitter) pool.
D000596:Amino Acids / Q000378:metabolism*; D000641:Ammonia / Q000378:metabolism; D000818:Animals; D001933:Brain Stem / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006501:Hepatic Encephalopathy / Q000378:metabolism*; D008297:Male; D009929:Organ Size; D011167:Portacaval Shunt, Surgical; D051381:Rats; D011919:Rats, Inbred Strains; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D000596:Amino Acids; D005680:gamma-Aminobutyric Acid; D000641:Ammonia; D005968:Glutamate Decarboxylase