Abstract: Parkinson’s disease is a chronic and progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta, which leads to the featured motor impairment of parkinsonism, including akinesia, bradykinesia, rigidity, and tremor (McGregor and Nelson, 2019). The natural progression of Parkinson’s disease can last for decades in humans, during which dopamine levels in the brain continue to drop as a consequence of the gradual degeneration of midbrain dopaminergic cells and their axonal projections to the striatum. At the same time, other parts of the brain adapt to the immediate consequences of the decreased dopamine levels. Some adaptations can act as compensatory mechanisms, delaying the onset of motor impairments. However, motor deficits become clinically noticeable when such adaptations fail to counteract the damages associated with the loss of dopamine. Over the last two decades, a series of adaptative changes at the molecular, cellular, and synaptic levels throughout the basal ganglia circuits have been reported (McGregor and Nelson, 2019; Chu, 2020). However, it remains undefined whether loss of dopamine also triggers similar adaptative changes in brain regions downstream of the basal ganglia.