The MPTP-treated mouse has proven to be a valuable model of parkinsonism. For example, C57 black mice treated with MPTP exhibit a large decrement in the neostriatal content of dopamine and its metabolites, a marked reduction in the capacity of neostriatal synaptosomal preparations to accumulate [3H]dopamine, a large decrease in neostriatal tyrosine hydroxylase activity, a marked loss of nerve cells in the zona compacta of the substantia nigra, and pronounced behavioral deficits. These biochemical, pathological and behavioral deficits are similarly observed in MPTP-treated primates and in humans with idiopathic parkinsonism. A great deal of our current knowledge concerning MPTP has come from experimentation carried out in the mouse.