By Todd Taylor & Michelle Jaffee
New mouse-model research by University of Florida neuroscientists provides fresh insight into the impact of elevated levels of the protein alpha-synuclein on the function of dopamine-producing nerve cells, the progressive demise of which is associated with Parkinson’s disease.
Using molecular biology, electrophysiology and live-cell imaging methods, the research team from the laboratories of Habibeh Khoshbouei, Ph.D., Pharm.D., and Benoit Giasson, Ph.D., report how excessive alpha-synuclein levels in dopamine neurons of mice disrupt multiple processes, including neuronal firing properties, calcium dynamics and dopamine release. The findings, published in the journal npj Parkinson’s Disease, are aimed to help guide development of future therapeutic approaches.
The researchers also reported that in mice, prolonged exposure to the drug quinpirole targeting the dopamine receptor D2R thwarts many of the disruptions induced by a-synuclein overexpression.
“Our research suggests that reducing the rate of neuronal loss in Parkinson’s disease could potentially be achievable by targeting this mechanism in earlier interventions,” Khoshbouei said. “We hope that this study will be an important step toward discovering better treatments to manage the clinical symptoms and progression of Parkinson’s disease.”