Parkinson disease is characterized by a complex neuropathological profile that primarily affects dopaminergic neural pathways in the basal ganglia, including pathways that modulate cranial sensorimotor functions such as swallowing, voice and speech. Prior work from our lab has shown that the rat model of unilateral 6-hydroxydopamine infusion to the medial forebrain bundle that is useful for studying limb sensorimotor deficits also yields vocalization deficits that may be amenable to treatment with intensive exercise. This affords us an opportunity to explore the potential mechanisms underlying behavioral and neural recovery as a result of intervention for cranial sensorimotor deficits associated with Parkinson disease. Our methods include recording and acoustic analysis of male rat ultrasonic vocalizations in a control condition, after neurotoxin infusion (Parkinson disease model), and after targeted vocalization training. We also use well-established behavioral and immunohistochemical methods to assess the level of neurochemical recovery in the striatum of the basal ganglia after our interventions. Our findings, although preliminary, prompt us to look in other brain regions extraneous to the striatum for potential underlying mechanisms of recovery. Thus, our future work will focus on the underlying mechanisms of behavioral recovery in a Parkinson disease model in the hope that this will lead to improved understanding of brain function and improved treatment for voice and swallowing disorders. Learning outcomes: Readers will gain an understanding of how a rat model of Parkinson disease is used to study vocalization deficits and interventions. (Contains 4 figures.)