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Growing evidence shows that dopamine depletion triggers network-level remodeling in the striatum, whose pathological significance extends far beyond acute changes in neuronal excitability. Striatal parvalbumin interneurons (PVINs) have recently been recognized as unique integrators of dopaminergic, neuroinflammatory and electrical network signals and as the principal striatal source of glial-cell-line-derived neurotrophic factor (GDNF). This integrative capacity renders PVINs early targets of parkinsonian injury, yet also allows them to orchestrate compensatory plasticity that shapes subsequent disease progression. Here we review how PVINs, via receptor-specific signaling, drive network reorganization in response to dopaminergic degeneration. We propose that these cells follow a compensatory-to-degenerative trajectory that canalizes abnormal synaptic plasticity and thereby exerts a maladaptive influence on PD pathogenesis. 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