Among symptoms characterizing Parkinson’s disease (PD), freezing of gait (FoG) can become particularly disabling for patients. Anxiety levels have been linked to the severity of FoG, yet in this circumstance, levodopa treatment lacks effectiveness. A better understanding of the neural circuit mechanisms underlying FoG is required for a more targeted approach towards its treatment. To this end, we developed a viral vector (AAV2/9-CreON-A53T-αSyn) mouse model restricting synucleinopathy to local circuit elements, i.e. selected neuron subtypes within specific brain regions in vivo. We validated this model by targeting dopaminergic (DA) neurons of the substantia nigra pars compacta (SNc). Our approach recapitulates main hallmarks of the disease, e.g. progressive cellular and nigrostriatal projections loss, and locomotor impairment. We then induced synucleinopathy specifically in noradrenergic cells of the locus coeruleus (NA-LC), a brain region implicated in anxiety behavior and affected by neurodegeneration in PD. We observed that mice display a heightened sensitivity to anxiogenic stimuli. Neuroanatomical tracing showed that NA-LC neurons project to the ventrolateral periaqueductal gray (vlPAG), a midbrain region important for defensive behavior, in particular freezing responses. Moreover, ex vivo slice electrophysiological recordings revealed that vlPAG glutamatergic and GABAergic neurons are modulated by LC inputs. In the framework of the reported defense circuitry, this would result in a decrease of the excitatory output, mediating freezing. Our data supports the notion that synucleinopathy-induced LC degeneration influences the activity of vlPAG circuits, leading to dysregulation of the defensive response. This circuit mechanism may contribute to the FoG phenomenon in PD.