Prodromal signs of Parkinson's disease (PD), including vocal communication deficits, are poorly understood and do not respond adequately to current pharmacologic treatments. Norepinephrine dysfunction is involved early in PD; thus, drug therapies targeting norepinephrine may be useful as a treatment of prodromal signs. This study used a validated, translational rodent model of prodromal PD, the male -/- rat, which exhibits ultrasonic vocalization (USV) deficits as early as 2 months of age. The purpose of this preclinical study was to investigate a dose-dependent (2.5, 5.0, 7.5, 10 mg/kg) response of methylphenidate on USV parameters with the hypothesis that methylphenidate would increase vocalization output. Because methylphenidate is a psychostimulant with known adverse side effects, we also hypothesized that potential side effects including anxietylike behavior and spontaneous activity would be increased in a dose-dependent manner. To accomplish this, wild-type (WT) and -/- rats were administered a dose of a vehicle (saline) and a methylphenidate dose in a randomized within-subjects design and then assessed for USVs, anxiety behavior (open field), and limb motor (cylinder) activity. The results suggest that methylphenidate does not alter USV emissions in -/- rats; however, methylphenidate increased the total number of vocalizations and duration of frequency-modulated calls in WT rats. Methylphenidate dose dependently influenced spontaneous movements in both WT and -/- rats, as expected, while methylphenidate increased anxiety in -/- rats and not WT rats. This study demonstrates a difference in response to a psychostimulant between -/- rats and WT rats. (PsycInfo Database Record (c) 2025 APA, all rights reserved).