English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

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

Tkac, I., Keene, C., 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(5), 891-898. doi:10.1002/jnr.10112.

Item is

Files

show Files

Locators

show
hide
Description:
-

Creators

show
hide
 Creators:
Tkac, I, Author
Keene, CD, Author
Pfeuffer, J1, Author              
Low, WC, Author
Gruetter, R, Author
Affiliations:
1External Organizations, ou_persistent22              

Content

show
hide
Free keywords: -
 Abstract: 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.

Details

show
hide
Language(s):
 Dates: 2001-12
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: BibTex Citekey: 2041
DOI: 10.1002/jnr.10112
 Degree: -

Event

show

Legal Case

show

Project information

show

Source 1

show
hide
Title: Journal of Neuroscience Research
  Other : J. Neurosci. Res.
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: Hoboken, NJ : Wiley-Liss, <2005->
Pages: - Volume / Issue: 66 (5) Sequence Number: - Start / End Page: 891 - 898 Identifier: ISSN: 0360-4012
CoNE: https://pure.mpg.de/cone/journals/resource/954925521676