Down regulation of striatal dopamine receptors in experimental hepatic encephalopathy.
Dopamine receptors were studied in striatal synaptosomes prepared from rat brain with hepatic encephalopathy induced by galactosamine-HCl and documented by visual evoked potential recordings. In order to further characterize the model, plasma amino acid levels and striatal catecholamines and octopamine levels were assayed. In agreement with previous reports in animal and in man, plasma amino acids were increased both in mild and severe stage of this pathology. Striatal levels of norepinephrine and dopamine fell during the development of coma while octopamine rose. Dopamine binding studies showed a decrease in the affinity during the mild stage and a reduction of receptor numbers in the severe stage of encephalopathy. The overall results, in the light of previous reports on GABA receptor studies, seem to indicate the presence in the development of encephalopathy of an imbalance between the dopaminergic and the GABAergic system leading to a prevalence of GABAergic inhibitory system.
D000596:Amino Acids / Q000097:blood; D000818:Animals; D002395:Catecholamines / Q000378:metabolism; D003342:Corpus Striatum / Q000378:metabolism*; D006501:Hepatic Encephalopathy / Q000378:metabolism*; D008297:Male; D009655:Octopamine / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000378:metabolism*; D013134:Spiperone / Q000378:metabolism; D014443:Tyrosine / Q000378:metabolism
D000596:Amino Acids; D002395:Catecholamines; D011954:Receptors, Dopamine; D009655:Octopamine; D014443:Tyrosine; D013134:Spiperone