Chronic intoxication with 3-nitropropionic acid in rats induces the loss of striatal dopamine terminals without
David Blum1, Marie-Christine Galas, Laetitia Cuvelier
1Laboratory of Neurophysiology, Université Libre de Bruxelles-Erasme, CP601, 808 route de Lennik, 1070 Brussels, Belgium. dablum@ulb.ac.be
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.


