In the brain, glycogen is primarily stored in astrocytes where it is regulated by several hormones /neurotransmitters including noradrenaline that controls glycogen breakdown (in the short term) and synthesis. Here we have examined the adrenoceptor (AR) subtype that mediates the glycogenic effect of noradrenaline in chick primary astrocytes by measurement of glycogen turnover (total (14) C incorporation of glucose into glycogen) following noradrenergic activation. Noradrenaline and insulin increased glycogen turnover in a concentration-dependent manner. The effect of noradrenaline was mimicked by stimulation of alpha(2) -ARs (and to a lesser degree by beta(3) -ARs), but not by stimulation of alpha(1) -, beta(1) - or beta(2) -ARs, and occurred only in astrocytes and not neurons. In chick astrocytes, studies using reverse transcription-polymerase chain reaction and radioligand binding showed that alpha(2A) - and alpha(2C) -AR mRNA and protein were present. alpha(2) -AR or insulin-mediated glycogen turnover was inhibited by phosphatidylinositol-3 kinase inhibitors, and both insulin and clonidine caused phosphorylation of Akt and glycogen synthase kinase-3 in chick astrocytes. alpha(2) -AR but not insulin-mediated glycogen turnover was inhibited by pertussis toxin pretreatment indicating involvement of Gi/o proteins. These results show that the increase in glycogen turnover caused by noradrenaline is due to activation of alpha(2) -ARs that increase glycogen turnover in astrocytes utilising a Gi/o-PI3K pathway.