Pandey, M., Mohanakumar, K., Usha, R. (2010). Striatal dopamine levels and changes in mitochondrial function following chronic 3-nitropropionic acid treatment in rats. Iranian Journal of Pharmaceutical Research, Volume 3(Supplement 1), 83-83.
M Pandey; KP Mohanakumar; R Usha. "Striatal dopamine levels and changes in mitochondrial function following chronic 3-nitropropionic acid treatment in rats". Iranian Journal of Pharmaceutical Research, Volume 3, Supplement 1, 2010, 83-83.
Pandey, M., Mohanakumar, K., Usha, R. (2010). 'Striatal dopamine levels and changes in mitochondrial function following chronic 3-nitropropionic acid treatment in rats', Iranian Journal of Pharmaceutical Research, Volume 3(Supplement 1), pp. 83-83.
Pandey, M., Mohanakumar, K., Usha, R. Striatal dopamine levels and changes in mitochondrial function following chronic 3-nitropropionic acid treatment in rats. Iranian Journal of Pharmaceutical Research, 2010; Volume 3(Supplement 1): 83-83.
Striatal dopamine levels and changes in mitochondrial function following chronic 3-nitropropionic acid treatment in rats
An irreversible inhibitor of complex II in the mitochondria, 3-nitropropionic acid (3-NP), induces bilateral striatal lesions with many neuropathological features of Huntington’s disease (HD) in rats. It is widely used as a model of HD. Chronic systemic treatment of 3-NP for 4 days in rats (10, 15 and 20 mg/kg) caused a significant dose-dependent reduction in succinate dehydrogenase activity, which was evident in histochemical as well as in biochemical assays. Splayed toes, and moderate to severe immobility in the hind limbs marked 3-NP administration in adult rats. A dose-dependent rise in striatal dopamine level, as measured employing HPLC-electrochemistry, was also evident. The rise in dopamine level was consistent in adult (4-6 months), but inconsistent in younger rats (2-3 months). A significant rise in NADH:ubiquinone reductase activity was indicated in the mitochondrial fractions prepared from the cerebral cortex region of rats treated with 3-NP. This was equally visible in the rotenone sensitive and insensitive fractions of the enzyme. Our results strongly suggest involvement of Complex I dysfunction in the behavioral and dopaminergic aberrations as seen in HD.
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