Methylglyoxal and carboxyethyllysine reduce glutamate uptake and S100B secretion in the hippocampus independently of RAGE activation.

Diabetes is a metabolic disease characterized by high fasting-glucose levels. Diabetic complications have been associated with hyperglycemia and high levels of reactive compounds, such as methylglyoxal (MG) and advanced glycation endproducts (AGEs) formation derived from glucose. Diabetic patients have a higher risk of developing neurodegenerative diseases, such as Alzheimer's disease or Parkinson's disease.

Effects of glyoxal or methylglyoxal on the metabolism of amino acids, lactate, glucose and acetate in the cerebral cortex of young and adult rats.

The in vitro effects of glyoxal and methylglyoxal on the metabolism of glycine, alanine, leucine, glutamate, glutamine, glucose, lactate and acetate were evaluated in cortico-cerebral slices from young (10-day-old) or adult (3-month-old) rats. In a first set of experiments with cortico-cerebral slices from young animals, the compounds glyoxal or methylglyoxal at 400 microM, increased the oxidation of alanine, leucine and glycine to CO(2) and decreased the protein synthesis from these amino acids. Lipid synthesis from alanine, leucine and glycine was not changed in the cortico-cerebral slices from young rats after glyoxals exposure.

Ontogenetic changes in glial fibrillary acid protein phosphorylation, glutamate uptake and glutamine synthetase activity in olfactory bulb of rats.

Phosphorylation of the glial fibrillary acidic protein (GFAP) in hippocampal and cerebellar slices from immature rats is stimulated by glutamate. This effect occurs via a group II metabotropic glutamate receptor in the hippocampus and an NMDA ionotropic receptor in the cerebellum. We investigated the glutamate modulation of GFAP phosphorylation in the olfactory bulb slices of Wistar rats of different ages (post-natal day 15 = P15, post-natal day 21 = P21 and post-natal day 60 = P60).