|Authors||Ciucci MR, Ma ST, Fox C, Kane JR, Ramig LO, Schallert T|
|Journal||Behav. Brain Res. Volume: 182 Issue: 2 Pages: 284-9|
|Publish Date||2007 Sep 4|
The sensorimotor speech/voice deficits associated with Parkinson disease have been well documented in humans. They are largely resistant to pharmacological and surgical treatment, but respond to intensive speech therapy. The mechanisms underlying this phenomenon are not well understood and are difficult to systematically test in humans. Thus, we turn to the rat as a model. The purpose of this study is to compare the ultrasonic vocalization (USV) of rats in three conditions: control, haloperidol-induced transient dopamine depletion, and unilateral 6-hydroxydopamine (6-OHDA) induced moderately-severe degeneration of dopamine neurons. It was hypothesized that both dopamine-altered conditions would lead to a change in the features of the USV acoustic signal. Results demonstrated that bandwidth decreased in the dopamine-altered rats. This is the first study to document a degradation of the acoustic signal of frequency-modulated 50-kHz calls as a result of interfering with dopamine synaptic transmission in rats. The data suggest that mild transient dopamine depletion with haloperidol or even unilateral degeneration of dopamine neurons is associated with changes in the USV acoustic signal. Dopaminergic dysfunction influences USV quality without reducing the number of calls. This study provides a foundation to examine the role of dopamine in sensorimotor processes underlying USV production and potentially to explore treatments for dopamine deficiency-related impaired vocal outcome.
|Full Text||Full text available on PubMed Central|