The presynaptic protein ¦Á-synuclein is central to the pathogenesis of ¦Á-synucleinopathies. We show that the presence of endogenous mouse ¦Á-synuclein leads to higher number of dopaminergic neurons in the substantia nigra of wild-type C57Bl/6J mice compared with C57Bl/6S mice with a spontaneous deletion of the ¦Á-synuclein gene or C57Bl/6J mice with a targeted deletion of the ¦Á-synuclein gene. This effect of ¦Á-synuclein on dopaminergic neuron occurs during development between E10.5 and E13.5 and persists in adult life supporting the involvement of ¦Á-synuclein in the development of a subset of dopaminergic neurons.