Parkinson’s disease (PD) is a progressive, degenerative disorder that affects 10 million people worldwide. More than 90% of individuals with PD develop hypokinetic dysarthria, a motor speech disorder that impairs vocal communication and quality of life. Despite the prevalence of vocal deficits in this population, very little is known about the pathological mechanisms underlying this aspect of disease. As such, effective treatment options are limited. Rat models have provided unique insights into the disease-specific mechanisms of vocal deficits in PD. This review summarizes recent studies investigating vocal deficits in 6-hydroxydopamine (6-OHDA), alpha-synuclein overex-pression, DJ1-/-, and Pink1-/-rat models of PD. Model-specific changes to rat ultrasonic vocalization (USV), and the effects of exercise and pharmacologic interventions on USV production in these models are discussed.
Bibliographical noteFunding Information:
Funding: This review was funded by the National Institutes of Health, grant number T32DC009401 (Krasko), R21 DC016135 (Kelm-Nelson); R01 NS117469 (Kelm-Nelson), R01 DC018584 (Ciucci), R01 DC014358 (Ciucci). The APC was funded by R01 DC018584 (Ciucci).
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
- Parkinson’s disease
- Ultrasonic vocalization
PubMed: MeSH publication types
- Journal Article