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- Title
Hyperhomocysteinemia reduces glutamate uptake in parietal cortex of rats
- Authors
Matté, Cristiane; Mussulini, Ben Hur M.; dos Santos, Tiago M.; Soares, Flávia M.S.; Simão, Fabrício; Matté, Aline; de Oliveira, Diogo L.; Salbego, Christianne G.; Wofchuk, Susana T.; Wyse, Angela T.S.
- Abstract
Abstract: In the present study we evaluated the effect of acute and chronic homocysteine administrations on glutamate uptake in parietal cortex of rats. The immunocontent of glial glutamate transporter (GLAST) and sodium-dependent glutamate/aspartate transporter (GLT-1) in the same cerebral structure was also investigated. For acute treatment, neonate or young rats received a single injection of homocysteine or saline (control) and were sacrificed 1, 8, 12h, 7 or 30 days later. For chronic treatment, homocysteine was administered to rats twice a day at 8h interval from their 6th to their 28th days old; controls and treated rats were sacrificed 12h, 1, 7 or 30 days after the last injection. Results show that acute hyperhomocysteinemia caused a reduction on glutamate uptake in parietal cortex of neonate and young rats, and that 12h after homocysteine administration the glutamate uptake returned to normal levels in young rats, but not in neonate. Chronic hyperhomocysteinemia reduced glutamate uptake, and GLAST and GLT-1 immunocontent. According to our results, it seems reasonable to postulate that the reduction on glutamate uptake in cerebral cortex of rats caused by homocysteine may be mediated by the reduction of GLAST and GLT-1 immunocontent, leading to increased extracellular glutamate concentrations, promoting excitotoxicity.
- Subjects
HOMOCYSTEINE; INJECTIONS; NEUROTRANSMITTER uptake inhibitors; GLUTAMIC acid; CEREBRAL cortex; LABORATORY rats
- Publication
International Journal of Developmental Neuroscience, 2010, Vol 28, Issue 2, p183
- ISSN
0736-5748
- Publication type
Article
- DOI
10.1016/j.ijdevneu.2009.11.004