beta2- and beta3-Adrenoceptors activate glucose uptake in chick astrocytes by distinct mechanisms: A mechanism for memory enhancement?

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Abstract

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.
Original languageEnglish
Pages (from-to)997 - 1008
Number of pages12
JournalJournal of Neurochemistry
Volume103
Issue number3
DOIs
Publication statusPublished - 2007

Cite this

@article{dd0a08c5cbd14eff86bbe16335e156f1,
title = "beta2- and beta3-Adrenoceptors activate glucose uptake in chick astrocytes by distinct mechanisms: A mechanism for memory enhancement?",
abstract = "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.",
author = "Hutchinson, {Dana Sabine} and Summers, {Roger James} and Gibbs, {Marie Elizabeth}",
year = "2007",
doi = "10.1111/j.1471-4159.2007.04789.x",
language = "English",
volume = "103",
pages = "997 -- 1008",
journal = "Journal of Neurochemistry",
issn = "0022-3042",
publisher = "Wiley-Blackwell",
number = "3",

}

beta2- and beta3-Adrenoceptors activate glucose uptake in chick astrocytes by distinct mechanisms: A mechanism for memory enhancement? / Hutchinson, Dana Sabine; Summers, Roger James; Gibbs, Marie Elizabeth.

In: Journal of Neurochemistry, Vol. 103, No. 3, 2007, p. 997 - 1008.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - beta2- and beta3-Adrenoceptors activate glucose uptake in chick astrocytes by distinct mechanisms: A mechanism for memory enhancement?

AU - Hutchinson, Dana Sabine

AU - Summers, Roger James

AU - Gibbs, Marie Elizabeth

PY - 2007

Y1 - 2007

N2 - 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.

AB - 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.

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JO - Journal of Neurochemistry

JF - Journal of Neurochemistry

SN - 0022-3042

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ER -