Regulation of Glycogenolysis in Transformed Astrocytes In Vitro

Abstract

Cultured [rat] astrocytes, transformed by Herpesvirus, were used as a model system to study several aspects of the control of glycogenolysis. Adrenergic agonists such as norepinephrine and isoproterenol caused an immediate and dose-dependent increase in the intracellular levels of cAMP. Concomitant with the initial phase of cAMP increase, conversion of phosphorylase b to a and glycogenolysis were observed. The elevation of cAMP, phosphorylase conversion, and glycogenolysis were simultaneously blocked by .beta.-adrenergic blockers, but not by .alpha.-adrenergic blocking agents. Repeated administration of norepinephrine caused an attenuated response in both cAMP accumulation and glycogenolysis. Glycogen degradation is also partially regulated by glucose availability. In the presence of glucose, norepinephrine-induced glycogenolysis is blocked, despite elevations in cAMP. The direct role of glucose is postulated, since glucose analogs mimic the effects of glucose.