Cerebral GABA-ergic and glutamatergic function in hepatic encephalopathy View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1987-02

AUTHORS

Roger F. Butterworth, Joël Lavoie, Jean-François Giguère, Gilles Pomier Layrargues, Marcelle Bergeron

ABSTRACT

Measurement of amino acids in brain tissue obtained at autopsy from cirrhotic patients dying in hepatic coma revealed a threefold increase in glutamine and a concomitant decrease in brain glutamate. The GABA levels were found to be unaltered. Studies using an animal model of portal-systemic encephalopathy gave similar results. Glutamic acid decarboxylase (GAD) activities were within normal limits, both in the brains of cirrhotic patients and portocaval-shunted rats. A previous study reported normal [3H]GABA binding to synaptic membrane preparations from cerebral cortex in these animals. Taken together, these findings suggest that cerebral GABA function is not impaired in hepatic encephalopathy associated with chronic liver disease and portal-systemic shunting. On the other hand, there is evidence to suggest that the releasable pool of glutamate may be depleted in brain in hepatic encephalopathy. Data consistent with this hypothesis include: Reduction in the evoked release of endogenous glutamate by superfusion of hippocampal slices with pathophysiological levels of ammonia; ammonia-induced reduction of glutamatergic neurotransmission; and an increase in the number of [3H]glutamate binding sites in synaptic membrane preparations from hyperammonemia rats and from rats with portocaval shunts. Such neurochemical changes may be of pathophysiological significance in hepatic encephalopathy. More... »

PAGES

131-144

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf02833603

DOI

http://dx.doi.org/10.1007/bf02833603

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1010746318

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/2888065


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