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Metabolic changes in quinolinic acid-lesioned rat striatum measured non-invasively by in vivo 1H NMR spectroscopy

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons84137

Keene CD, Pfeuffer,  J
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Zitation

Tkac, I., Keene CD, Pfeuffer, J., Low, W., & Gruetter, R. (2001). Metabolic changes in quinolinic acid-lesioned rat striatum measured non-invasively by in vivo 1H NMR spectroscopy. Journal of Neuroscience Research, 66, 891-898. Retrieved from http://www3.interscience.wiley.com/cgi-bin/abstract/88511374/START.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0013-E338-D
Zusammenfassung
Intrastriatal injection of quinolinic acid (QA) provides an animal model of Huntington disease. In vivo (1)H NMR spectroscopy was used to measure the neurochemical profile non-invasively in seven animals 5 days after unilateral injection of 150 nmol of QA. Concentration changes of 16 metabolites were measured from 22 microl volume at 9.4 T. The increase of glutamine ((+25 +/- 14), mean +/- SD, n = 7) and decrease of glutamate (-12 +/- 5), N-acetylaspartate (-17 +/- 6), taurine (-14 +/- 6) and total creatine (-9 +/- 3) were discernible in each individual animal (P < 0.005, paired t-test). Metabolite concentrations in control striata were in excellent agreement with biochemical literature. The change in glutamate plus glutamine was not significant, implying a shift in the glutamate-glutamine interconversion, consistent with a metabolic defect at the level of neuronal-glial metabolic trafficking. The most significant indicator of the lesion, however, were the changes in glutathione ((-19 +/- 9), P < 0.002)), consistent with oxidative stress. From a comparison with biochemical literature we conclude that high-resolution in vivo (1)H NMR spectroscopy accurately reflects the neurochemical changes induced by a relatively modest dose of QA, which permits one to longitudinally follow mitochondrial function, oxidative stress and glial-neuronal metabolic trafficking as well as the effects of treatment in this model of Huntington disease.