Journal
NEUROCHEMICAL RESEARCH
Volume 34, Issue 7, Pages 1261-1271Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-008-9904-5
Keywords
N-Acetylaspartate (NAA); N-Acetylaspartylglutamate (NAAG); gamma-Amino-butyric acid (GABA); Choline; Huntington's disease (HD); Magic-angle-spinning (MAS); Metabonomics; Mitochondria; NMR spectroscopy; 3-Nitropropionic acid (3-NP); Succinate
Categories
Ask authors/readers for more resources
3-Nitropropionic acid (3-NP)-induced neurotoxicity can be used as a model for the genetic neurodegenerative disorder Huntington's disease (HD). A metabolic profiling strategy was adopted to explore the biochemical consequences of 3-NP administered to rats in specific brain regions. H-1 NMR spectroscopy was used to characterize the metabolite composition of several brain regions following 3-NP-intoxication. Dose-dependent increases in succinate levels were observed in all neuroanatomical regions, resulting from the 3-NP-induced inhibition of succinate dehydrogenase. Global decreases in taurine and GABA were observed in the majority of brain regions, whereas altered lipid profiles were observed only in the globus pallidus and dorsal striatum. Depleted phosphatidylcholine and elevated glycerol levels, which are indicative of apoptosis, were also observed in the frontal cortex of the 3-NP model. Many of the metabolic anomalies are consistent with those reported in HD. The 3-NP-induced model of HD provides a means of monitoring potential mechanisms of pathology and therapeutic response for drug interventions, which can be efficiently assessed using metabolic profiling strategies.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available