Ceftriaxone-induced up-regulation of cortical and striatal GLT1 in the R6/2 model of Huntington's disease |
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| Authors: | Youssef Sari Anne L Prieto Scott J Barton Benjamin R Miller George V Rebec |
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| Affiliation: | (1) Program in Neuroscience, Indiana University, 1101 East 10th Street, Bloomington, IN, USA;(2) Department of Psychological and Brain Sciences, Indiana University, 1101 East 10th Street, Bloomington, IN, USA;(3) College of Pharmacy, Department of Pharmacology, Health Science Campus, University of Toledo, 3000 Arlington Avenue, 43606 Toledo, OH, USA;(4) Department of Physiology, University of Texas Southwestern Medical School, 5323 Harry Hines Boulevard, 75390 Dallas, TX, USA |
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| Abstract: | Background Huntington's disease (HD) is an inherited neurodegenerative disorder characterized by cortico-striatal dysfunction and loss of glutamate uptake. At 7 weeks of age, R6/2 mice, which model an aggressive form of juvenile HD, show a glutamate-uptake deficit in striatum that can be reversed by treatment with ceftriaxone, a β-lactam antibiotic that increases GLT1 expression. Only at advanced ages (> 11 weeks), however, do R6/2 mice show an actual loss of striatal GLT1. Here, we tested whether ceftriaxone can reverse the decline in GLT1 expression that occurs in older R6/2s. |
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