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.