Though many neuronal populations are affected in Parkinson’s disease (PD), its cardinal motor symptoms are a consequence of dopamine (DA) neuron loss in the substantia nigra (SNc). The precise mechanisms underlying DA neuron vulnerability remain unclear, but include oxidative stress, and aggregation of alpha-synuclein. More recently, a glutamate driven process has been implicated in disease progression, and there is now proof that DA neurons express the vesicular glutamate transporter VGLUT2 and co-release glutamate. In fact, we discovered that the majority of midbrain DA neurons transiently express VGLUT2 in development, but most shut down expression in the adult. Interestingly, DA neurons expressing VGLUT2 were shown to be more protected in various models of PD and are enriched in the SNc of human PD patients suggesting that VGLUT2 confers neuroprotective properties. However, it remains unclear whether DA neurons already expressing VGLUT2 are simply selected over non-VGLUT2 DA neurons, and/or whether VGLUT2 expression can also re-emerge in DA neurons not expressing VGLUT2 prior to neuronal injury. Using several pharmacological mouse models of reversible parkinsonism, we show that transient DA depletion or inhibition of DA receptors can lead to re-emergence of VGLUT2 in subsets of DA neurons without concomitant DA neuron loss. This suggests that pharmacological treatments that upregulate VGLUT2 expression in DA neurons may protect against PD.