Effect of acute hepatic encephalopathy on [H-3]dopamine release from rat cerebral cortex and striatum in vitro: role of Ca2+

Hepatic encephalopathy (HE) is characterized by motor symptoms associated w ith disturbed functions of the dopaminergic systems, but the underlying mec hanisms are not clear. A previous study from our laboratories revealed that HE, induced in rats by repeated treatment with thioacetamide, enhanced the 50 mM potassium (KCl) -stimulated release of newly loaded [H-3]dopamine in both striatal and frontal cerebral cortical slices in the presence of Ca2. In the present study we compared the effects of RE on dopamine release in striatal and frontal cerebral cortical slices and synaptosomes in the pres ence and absence of Ca2+. HE enhanced the KCl-stimulated [H-3]dopamine rele ase from striatal and frontal cortical synaptosomes in the presence of Ca2 to the same extent as in slices prepared from the respective brain regions . In the absence of Ca2+ a slight reduction in dopamine release was observe d in frontal cortical synaptosomes from HE rats when compared to control ra ts, while no effect of HE on the release was discernible in frontal cortica l and striatal slices and striatal synaptosomes. We conclude that in both b rain regions studied HE stimulates dopamine exocytosis triggered by Ca2+ in flux without affecting the release mediated by means of plasma membrane tra nsporters or exocytosis involving intraterminal Ca2+.