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dc.contributor.authorFonseca, Carla P.-
dc.contributor.authorSierra, Alejandra-
dc.contributor.authorGeraldes, Carlos F. G. C.-
dc.contributor.authorCerdán, Sebastián-
dc.contributor.authorCastro, M. Margarida C. A.-
dc.date.accessioned2013-09-24T09:28:45Z-
dc.date.available2013-09-24T09:28:45Z-
dc.date.issued2009-
dc.identifierdoi: 10.1002/jnr.21900-
dc.identifierissn: 0360-4012-
dc.identifiere-issn: 1097-4547-
dc.identifier.citationJournal of Neuroscience Research 87(4): 1046-1055 (2009)-
dc.identifier.urihttp://hdl.handle.net/10261/82624-
dc.description.abstractWe investigated by 13C nuclear magnetic resonance (NMR) the mechanisms underlying Li+ effects on glutamatergic and GABAergic neurotransmission systems in the adult rat brain and in primary cultures of cortical neurons and astrocytes during the metabolism of (1-13C) glucose or (2-13C) acetate. Adult male rats receiving a single dose of Li+ intraperitoneally (7 mmol/kg) were infused 2 hr later, for 60 min, with (1-13C) glucose (80 μmol/min/kg) or (2-13C) acetate (240 μmol/min/ kg). High-resolution 13C NMR spectra of brain extracts prepared after the infusion revealed that Li+ significantly decreased the incorporation of 13C in glutamate and GABA (γ-aminobutyric acid) carbons from (1-13C) glucose, but not from (2-13C) acetate. To complement the in vivo approach, primary cultures of cortical neurons or astrocytes were incubated with 1 mM uniformly 13C-labeled glucose or 5 mM (2-13C) acetate, in the absence and presence of increasing Li+ concentrations up to 15 mM. Under these conditions, Li1 significantly decreased neuronal glucose uptake in a concentration-dependent manner without apparent effects on astrocytic acetate uptake. Extracts prepared at the end of the incubations showed that Li+ significantly decreased the incorporation of 13C labeling into GABA carbons from its precursor glutamate in neurons, but such a decrease into glutamine carbons in astrocytes was not statistically significant. Our results indicate that the effects of Li+ are mediated through a reduction of neuronal glucose uptake, resulting in a decrease of glutamatergic and GABAergic neurotransmission without apparent effects on astrocytic metabolism. © 2008 Wiley-Liss, Inc.-
dc.description.sponsorshipFunded by: Fundação para a Ciência e a Tecnologia (F.C.T.), Portugal and FEDER. Grant Numbers: POCTI/1999/BCI/36160, PRAXIS XXI/BD/21462/99; Spanish Ministry of Education and Science. Grant Numbers: SAF 2001-2245, SAF 2004-03197; Institute of Health Carlos III. Grant Numbers: FISss C03/08, C03/155, C03/10, PI051530, PI051845 and Community of Madrid, Spain.-
dc.language.isoeng-
dc.publisherWiley-Blackwell-
dc.rightsclosedAccess-
dc.titleMechanisms underlying Li+ effects in glutamatergic and GABAergic neurotransmissions in the adult rat brain and in primary cultures of neural cells as revealed by 13C NMR-
dc.typeartículo-
dc.identifier.doihttp://dx.doi.org/10.1002/jnr.21900-
dc.date.updated2013-09-24T09:28:45Z-
dc.description.versionPeer Reviewed-
dc.contributor.funderFundação para a Ciência e a Tecnologia (Portugal)-
dc.contributor.funderInstituto de Salud Carlos III-
dc.contributor.funderMinisterio de Educación y Ciencia (España)-
dc.contributor.funderComunidad de Madrid-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100001871es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100012818es_ES
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