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Up‐regulation of glutamate concentration in the putamen and in the prefrontal cortex of asymptomatic SIVmac251‐infected macaques without major brain involvement
Author(s) -
Bossuet Christophe,
Vaufrey Françoise,
Condé Françoise,
Chrétien Fabrice,
Pichon Jacques,
Hantraye Philippe,
Le Grand Roger,
Dormont Dominique,
Gras Gabriel
Publication year - 2004
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2003.02237.x
Subject(s) - glutamate receptor , endocrinology , medicine , glutamine , prefrontal cortex , gliosis , biology , creatine , taurine , choline , biochemistry , neuroscience , amino acid , receptor , cognition
We quantified putamen and prefrontal cortex metabolites in macaques with simian immunodeficiency virus infection and searched for virological and histological correlates. Fourteen asymptomatic macaques infected since 8–78 months (median: 38) were compared with eight uninfected ones. Absolute concentrations of acetate, alanine, aspartate, choline, creatine, GABA, glutamate, glutamine, lactate, myo‐inositol, N ‐acetylaspartate, taurine and valine were determined by ex vivo proton magnetic resonance spectroscopy. Glutamate concentration in the CSF was determined by HPLC. Gliosis was assessed by glial fibrillary acidic protein and CD68 immunohistochemistry. Glutamate concentration was slightly increased in the prefrontal cortex (19%, p = 0.0152, t ‐test) and putamen (13%, p = 0.0354, t ‐test) of the infected macaques, and was unaffected in the CSF. Myo‐inositol concentration was increased in the prefrontal cortex only (27%, p = 0.0136). The concentrations of glutamate and myo‐inositol in the prefrontal cortex were higher in the animals with marked or intense microgliosis ( p = 0.0114). The other studied metabolites, including N ‐acetylaspartate, were not altered. Glutamate concentration may thus increase in the cerebral parenchyma in asymptomatic animals, but is not accompanied by a detectable decrease in N ‐acetylaspartate concentration (neuronal dysfunction). Thus, there are probably compensatory mechanisms that may limit glutamate increase and/or counterbalance its effects.