Abstract
3-Nitropropionic acid (3NP) is a succinate dehydrogenase inhibitor allowing the generation of animal models of Huntington's disease. In the present study, we found that a 5-day continuous chronic infusion of 3NP produces loss of [ 3H]mazindol binding and tyrosine hydroxylase (TH) immunoreactivity in the striatal area of degeneration. This loss of dopamine terminals was not due to a loss of nigral neurons since the expression of TH as well as the number of TH-expressing neurons remained unaltered in the substantia nigra of rats treated by 3NP. This suggests that the 3NP-induced dopamine terminal loss is secondarily related to the striatal degeneration andlor to a direct effect of 3NP on striatal terminals and not to a primary effect on nigral cells.
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