Brain cholecystokinin and vasoactive intestinal polypeptide: immunoreactivity in rabbits with hepatic coma.
Recent studies have suggested that decreased excitatory neurotransmission in the brain may contribute to the overall neural inhibition which characterizes the syndrome of hepatic encephalopathy (HE), and that vasoactive intestinal polypeptide (VIP) and cholecystokinin (CCK) may promote neural excitation in the brain. To determine if brain levels of these neuropeptides are altered in HE, measurements were made of the concentrations of immunoreactive VIP (iVIP) and immunoreactive CCK (iCCK) in cerebral cortex, cerebellum and hypothalamus isolated from normal rabbits and rabbits with galactosamin-induced hepatic coma. Hepatic coma was associated with reduced concentrations of iVIP, small molecular weight iCCK and large molecular weight iCCK in the cerebral cortex but not in the cerebellum or hypothalamus. These findings are compatible with decreased VIP- and CCK-mediated neural excitation occurring in the syndrome of HE.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002531:Cerebellum / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism; D002766:Cholecystokinin / Q000378:metabolism*; D005688:Galactosamine; D006501:Hepatic Encephalopathy / Q000139:chemically induced / Q000378:metabolism*; D007031:Hypothalamus / Q000378:metabolism; D008970:Molecular Weight; D011817:Rabbits; D014660:Vasoactive Intestinal Peptide / Q000378:metabolism*
D014660:Vasoactive Intestinal Peptide; D005688:Galactosamine; D002766:Cholecystokinin