Loss of GABAB binding sites in the cerebral cortex of rats with acute hepatic encephalopathy.
The binding of [3H]GABA to GABAA and GABAB binding sites was measured in cerebral cortical membranes derived from control rats and rats with acute hepatic encephalopathy (HE) induced with a hepatotoxin, thioacetamide. HE did not affect the kinetic parameters (KD and Bmax) for the GABAA binding site. However, HE decreased Bmax (but not KD) for the GABAB binding site to 32% of the control level, indicating a substantial loss of GABAB receptors. Since GABAB receptors control the cerebral cortical release of the amino acid neurotransmitters glutamate and GABA, the loss of GABAB receptors is likely to contribute to the array of disturbances of glutamatergic and GABAergic neurotransmission known to accompany HE.
Oja
S S
SS
Department of Biomedical Sciences, University of Tampere, Finland.
Saransaari
P
P
Wysmyk
U
U
Albrecht
J
J
D000208:Acute Disease; D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism*; D006501:Hepatic Encephalopathy / Q000139:chemically induced / Q000378:metabolism*; D066298:In Vitro Techniques; D007700:Kinetics; D008297:Male; D008566:Membranes / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011963:Receptors, GABA-A / Q000378:metabolism; D018080:Receptors, GABA-B / Q000378:metabolism*; D013853:Thioacetamide; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D011963:Receptors, GABA-A; D018080:Receptors, GABA-B; D013853:Thioacetamide; D005680:gamma-Aminobutyric Acid