Abstract
l-Deprenyl, a monoamine oxidase B (MAO-B) inhibitor, administered prior to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) protects dopaminergic neurons against degeneration in several animal species including mice. l-Deprenyl inhibits MPP + formation, the mediator of MPTP toxicity. In addition, l-deprenyl, administered 72 h following MPTP, improves the recovery of tyrosine hydroxylase (TH) immunopositive neurons in the substantia nigra (SN) of mice. This observation lead to the proposal that l-deprenyl exerts a `neurorescue' effect. However, clinical trials failed to demonstrate that l-deprenyl can effectively `rescues' degenerating dopaminergic neurons in early untreated Parkinson's disease (PD) patients. These observations prompted us to reevaluate the long-term impact of l-deprenyl on MPTP-induced dopaminergic cell loss in mice. In addition, we made use of another MAO-B inhibitor, MDL72974, to assess MAO-B participation in this paradigm. Our results suggest that l-deprenyl does not improve the recovery of TH immunopositive neurons in MPTP-treated mice. An apparent reduction in TH + neurons is observed in the SN of MDL72974 and l-deprenyl/MPTP-treated mice at 30 days post-treatment. The possible implication of these findings in relation to the used of MAO-B inhibitors in PD is discussed.
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