Isoprenaline, acting at beta-adrenoceptors (ARs), enhances memory formation in single trial discriminated avoidance learning in day-old chicks by mechanisms involving alterations in glucose and glycogen metabolism. Earlier studies of memory consolidation in chicks indicated that beta(3)-ARs enhanced memory by increasing glucose uptake, whereas beta(2)-ARs enhance memory by increasing glycogenolysis. This study examines the ability of beta-ARs to increase glucose uptake in chick forebrain astrocytes. The beta-AR agonist isoprenaline increased glucose uptake in a concentration-dependent manner, as did insulin. Glucose uptake was increased by the beta(2)-AR agonist zinterol and the beta(3)-AR agonist CL316243, but not by the beta(1)-AR agonist RO363. In chick astrocytes, reverse transcription-polymerase chain reaction studies showed that beta(1)-, beta(2)-, and beta(3)-AR mRNA were present, whereas radioligand-binding studies showed the presence of only beta(2)- and beta(3)-ARs. beta-AR or insulin-mediated glucose uptake was inhibited by phosphatidylinositol-3 kinase and protein kinase C inhibitors, suggesting a possible interaction between the beta-AR and insulin pathways. However beta(2)- and beta(3)-ARs increase glucose uptake by two different mechanisms: beta(2)-ARs via a Gs-cAMP-protein kinase A-dependent pathway, while beta(3)-ARs via interactions with Gi. These results indicate that activation of beta(2)- and beta(3)-ARs causes glucose uptake in chick astrocytes by distinct mechanisms, which may be relevant for memory enhancement.