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Mechanisms 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

AuthorsFonseca, Carla P.; Sierra, Alejandra CSIC ORCID; Geraldes, Carlos F. G. C.; Cerdán, Sebastián CSIC ORCID; Castro, M. Margarida C. A.
Issue Date2009
CitationJournal of Neuroscience Research 87(4): 1046-1055 (2009)
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.
Identifiersdoi: 10.1002/jnr.21900
issn: 0360-4012
e-issn: 1097-4547
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