Freezing of Gait (FoG) is a debilitating symptom of Parkinson´s Disease (PD) with unknown neural origin that is characterized by sudden gait disruption. A subgroup of FoG-patients is specifically sensitive to anxiety stimuli and states. Similar behavioral patterns relating anxiety and gait interruption can be found in defensive freezing of rodents where a disinhibitory mechanism within the ventrolateral periaqueductal gray (vlPAG) generates gait disruption and subsequent immobility due to threat.Classical rodent behavioral paradigms binarize anxiety states based on clear separation of anxiogenic and non-anxiogenic areas. However, to better understand different sensitivities to anxiogenic stimuli, a more graded effect of anxiogenic stimuli needs to be modeled.Here, we introduce a novel translational paradigm, the Opening Track (OT), in which openness is used as an anxiogenic stimulus for mice, and gradually increases along a linear track.To address potential causes underlying FoG, we used OT to assess how cell type-specific synucleinopathy in dopaminergic substantia nigra pars compacta (DA-SNc) or noradrenergic locus coeruleus (NA-LC) neurons affects gait disruption and its relation with the progressively increasing anxiogenic stimuli. Mice with DA-SNc or NA-LC synucleinopathy exhibited more gait disruptions in less open (and thus less anxiogenic) areas of OT. Whereas this can be explained by motor impairment for mice with DA-SNc neurodegenration, NA-LC synucleinopathy results in heightened sensitivity to anxiogenic stimuli. Together, the OT paradigm and cell type-specific synucleinopathy support our understanding of how circuit alterations in PD affect the interplay of anxiety states and gait behavior.