Vocal communication impairment and anxiety are co-occurring and interacting signs of Parkinson Disease (PD) that are common, poorly understood, and under-treated. Both vocal communication and anxiety are influenced by the locus coeruleus noradrenergic system. In light of this shared neural substrate and considering that noradrenergic dysfunction is a defining characteristic of PD, tandem investigation of vocal impairment and anxiety in PD relative to noradrenergic mechanisms is likely to yield insights into the disease-specific causes of these impairments. To address this gap in knowledge, we assessed vocal impairment and anxiety behavior relative to norepinephrine in a genetic rat model of early-onset PD (Pink1-/-). In Study 1, Pink1-/- rats and wild type controls (WT) underwent testing of ultrasonic vocalization and anxiety behavior at 4, 8, and 12 months of age. At 12 months of age, brainstem norepinephrine markers were analyzed with immunohistochemistry. We hypothesized that 1) anxiety would be increased in Pink1-/- rats, 2) vocal deficits and anxiety would be correlated to one another, 3) noradrenergic markers in the brainstem would be disrupted in Pink1-/-, and 4) brainstem noradrenergic markers would be associated with vocal acoustic changes and anxiety level. Results demonstrated that vocal impairment and anxiety were increased in Pink1-/- rats, and increased anxiety was associated with greater vocal deficit. Further, brainstem noradrenergic markers differed by genotype, and were associated with vocalization and anxiety behavior. In Study 2, we assessed the influence of pharmacologic manipulation of noradrenergic systems on vocal impairment and anxiety in the Pink1-/- rat model of PD. Anxiety behavior on the elevated plus maze and ultrasonic vocalizations were tested twice for each rat: once after injection of saline and once after administration of one of the three drugs. We hypothesized that norepinephrine reuptake inhibitors (atomoxetine and reboxetine) and a receptor antagonist (propranolol) would decrease vocal impairment and anxiety compared to saline. Our results demonstrated that both atomoxetine and reboxetine decreased anxiety. Atomoxetine also modulated acoustic parameters of ultrasonic vocalization, including increases in call intensity. Collectively, these studies demonstrate significant relationships among vocal impairment, anxiety and central noradrenergic systems in the Pink1-/- rat model of PD.