The neural mechanisms underlying vocal motor control are poorly understood in mammalian systems. Particularly lacking are details pertaining to the mechanisms and neuroanatomical basis of sensory-motor integration and vocal plasticity, both of which are thought to be essential for evolutionarily advanced vocal behaviors like birdsong or human speech. Based on clinical evidence and imaging studies in humans, as well as its known significance for motor control in general, the basal ganglia (BG) have been hypothesized as a key site for audio-vocal integration, but direct evidence of this is lacking. In this dissertation, I will fill this gap by providing experimental evidence that the basal ganglia are an important component of the forebrain vocal motor pathway. First, I present two examples of vocal plasticity in Tadarida brasiliensis that can serve as powerful behavioral assays of audio-vocal integration. Secondly I provide evidence of BG functions in audio-vocal integration by knocking down striatal dopamine levels with the neurotoxin 1-methyl-4-phenyl-1,2,3,6 tetrahydropyrridine (MPTP). Finally, I will utilize the D1-type receptor specific agonist SKF82958 and antagonist SCH23390 to examine how the direct pathway of the BG regulates vocal production and sensorymotor integration. The behavioral results of these experiments indicate that the bats have a complex and context depended vocal response to noise stimuli that can be used to examine the neurological control of vocal plasticity. Further, the pharmacological evidence demonstrated that the BG was necessary for maintaining and modulating normal muscle force during vocal production. Finally, the mechanism of action in the basal ganglia was found to depend at least partly on activity at D1-type dopamine receptors. The results of this dissertation support the hypothesis that the BG is a critical structure in the modulation of vocal commands in the forebrain vocal-motor pathway. Pathological or pharmacological disruption of dopamine signaling severely degraded the bats abilities to produce natural sounding calls or make adaptive changes to the acoustic environment. These results have implications for research into the treatment of basal ganglia disorders such as Parkinson’s disease, providing an animal model for the study of hypokinetic dysarthria.

PURPOSE: Vocal hyperfunction (VH) is considered a functional voice disorder, resulting in voice complaints of hoarseness and fatigue; however, recent work suggests that voice changes in VH may result from impairments in the neural control of voice (specifically, how voice perception is integrated into voice production). This study sought to clarify whether impaired auditory acuity of vocal pitch and the temporal production of voice, two known impairments in speakers with VH, were correlated. METHOD: The current study included 29 adults with VH. Vocal auditory perception was assessed via acuity to self-produced vocal pitch (quantified using an adaptive two-forced-choice paradigm). To investigate temporal acoustic measures of voice production, voice onset time (VOT) variability of voiced and voiceless stop consonants in a carrier phrase were separately assessed using a coefficient of variation (CoV). Two Pearson product-moment correlations were completed to assess the relationship between these measures of vocal perception and vocal production of either voiced or voiceless VOTs. RESULTS: No statistically significant correlations were observed between auditory acuity and CoV of VOT for neither voiced nor voiceless stop consonants. CONCLUSION: The current findings suggest that impairments in vocal pitch acuity and VOT production in VH are not governed by the same underlying mechanism. Further investigation is recommended to determine the etiology driving these vocal perception- and production-based impairments observed in prior work.