alpha{2}-Adrenoceptors activate noradrenaline-mediated glycogen turnover in chick astrocytes

Dana Sabine Hutchinson, Stephanie L Catus, Jon Merlin, Roger J Summers, Marie E Gibbs

Research output: Contribution to journalArticleResearchpeer-review

Abstract

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.
Original languageEnglish
Pages (from-to)915 - 926
Number of pages12
JournalJournal of Neurochemistry
Volume117
Issue number5
DOIs
Publication statusPublished - 2011

Cite this

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title = "alpha{2}-Adrenoceptors activate noradrenaline-mediated glycogen turnover in chick astrocytes",
abstract = "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.",
author = "Hutchinson, {Dana Sabine} and Catus, {Stephanie L} and Jon Merlin and Summers, {Roger J} and Gibbs, {Marie E}",
year = "2011",
doi = "10.1111/j.1471-4159.2011.07261.x",
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pages = "915 -- 926",
journal = "Journal of Neurochemistry",
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alpha{2}-Adrenoceptors activate noradrenaline-mediated glycogen turnover in chick astrocytes. / Hutchinson, Dana Sabine; Catus, Stephanie L; Merlin, Jon; Summers, Roger J; Gibbs, Marie E.

In: Journal of Neurochemistry, Vol. 117, No. 5, 2011, p. 915 - 926.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - alpha{2}-Adrenoceptors activate noradrenaline-mediated glycogen turnover in chick astrocytes

AU - Hutchinson, Dana Sabine

AU - Catus, Stephanie L

AU - Merlin, Jon

AU - Summers, Roger J

AU - Gibbs, Marie E

PY - 2011

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N2 - 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.

AB - 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.

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