Abnormal bursting as a pathophysiological mechanism in Parkinson's disease

• Type of Material: Article
• Authors: Collin J. Lobb, Emory University
• Language: English
• Date: 2014-04
• Publisher: Elsevier: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2013 Elsevier GmbH. All rights reserved.
• Final Published Version (URL): http://dx.doi.org/10.1016/j.baga.2013.11.002
• Title of Journal or Parent Work: Basal Ganglia
• ISSN: 2210-5336
• Volume: 3
• Issue: 4
• Start Page: 187
• End Page: 195
• Grant/Funding Information: Funding sources: P50NS071669, F32NS080589
• Keywords: burst; Parkinson's disease; basal ganglia
• Research Categories: Biology, Neuroscience

Abstract

Despite remarkable advances in Parkinson's disease (PD) research, the pathophysiological mechanisms causing motor dysfunction remain unclear, possibly delaying the advent of new and improved therapies. Several such mechanisms have been proposed including changes in neuronal firing rates, the emergence of pathological oscillatory activity, increased neural synchronization, and abnormal bursting. This review focuses specifically on the role of abnormal bursting of basal ganglia neurons in PD, where a burst is a physiologically-relevant, transient increase in neuronal firing over some reference period or activity. After reviewing current methods for how bursts are detected and what the functional role of bursts may be under normal conditions, existing studies are reviewed that suggest that bursting is abnormally increased in PD and that this increases with worsening disease. Finally, the influence of therapeutic approaches for PD such as dopamine-replacement therapy with levodopa or dopamine agonists, lesions, or deep brain stimulation on bursting is discussed. Although there is insufficient evidence to conclude that increased bursting causes motor dysfunction in PD, current evidence suggests that targeted investigations into the role of bursting in PD may be warranted.