Enhanced GABA release in cerebral cortical slices derived from rats with thioacetamide-induced hepatic encephalopathy.
The release of newly loaded [3H]GABA was studied in slices of different brain regions derived from rats in which acute hepatic encephalopathy (HE) was induced with a hepatotoxin thioacetamide. HE increased both spontaneous and high (50 mM) ammonium chloride-evoked GABA release in cerebral cortical slices by 38% and 50%, respectively. No effects of HE were noted in cerebellar or striatal slices. An increased release of GABA in the cerebral cortex may contribute to the endogenous benzodiazepine-mediated enhancement of GABAergic tone, which is thought to be partly responsible for the pathophysiological mechanism of HE.
Wysmyk
U
U
Department of Biomedical Sciences, University of Tampere, Finland.
Oja
S S
SS
Saransaari
P
P
Albrecht
J
J
D000643:Ammonium Chloride / Q000494:pharmacology; D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D006501:Hepatic Encephalopathy / Q000139:chemically induced / Q000503:physiopathology*; D007700:Kinetics; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013853:Thioacetamide; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D000643:Ammonium Chloride; D013853:Thioacetamide; D005680:gamma-Aminobutyric Acid