Titre
A2B receptor activation promotes glycogen synthesis in astrocytes through modulation of gene expression.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Auteur(s)
Allaman, I.
Auteure/Auteur
Lengacher, S.
Auteure/Auteur
Magistretti, P.J.
Auteure/Auteur
Pellerin, L.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
0363-6143
Statut éditorial
Publié
Date de publication
2003-03
Volume
284
Numéro
3
Première page
C696
Dernière page/numéro d’article
C704
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Résumé
Adenosine has been proposed as a key factor regulating the metabolic balance between energy supply and demand in the central nervous system. Because astrocytes represent an important cellular element in the control of brain energy metabolism, we investigated whether adenosine could induce long-term changes of glycogen levels in primary cultures of mouse cortical astrocytes. We observed that adenosine increased glycogen content, up to 300%, in a time- (maximum at 8 h) and concentration-dependent manner with an EC(50) of 9.69 microM. Pharmacological experiments using the broad-spectrum agonist 5'-(N-ethylcarboxamido)adenosine (NECA) and specific agonists for the A(1), A(2A), and A(3) receptors [N(6)-cyclopentyladenosine (CPA), CGS-21680, and IB-MECA, respectively] suggest that the effect of adenosine is mediated through activation of the low-affinity A(2B) adenosine receptor subtype. Interestingly, adenosine induces in parallel the expression of the protein targeting to glycogen (PTG), one of the protein phosphatase-1 glycogen-targeting subunits that has been implicated in the control of glycogen levels in various tissues. These results indicate that adenosine can exert long-term control over glycogen levels in astrocytes and might therefore play a significant role in physiological and/or pathological processes involving long-term modulation of brain energy metabolism.
Sujets
PID Serval
serval:BIB_CC56A622ABF8
PMID
Date de création
2008-01-24T12:17:07.774Z
Date de création dans IRIS
2025-05-21T00:19:50Z