Abstract
The mechanisms for the emergence and transmission of synchronized oscillations in Parkinson's disease, which are potentially causal to motor deficits, remain debated. Aside from the motor cortex and the subthalamic nucleus, the external globus pallidus (GPe) has been shown to be essential for the maintenance of these oscillations and plays a major role in sculpting neural network activity in the basal ganglia (BG). While neural activity of the healthy GPe shows almost no correlations between pairs of neurons, prominent synchronization in the β frequency band arises after dopamine depletion. Several studies have proposed that this shift is due to network interactions between the different BG nuclei, including the GPe. However, recent studies demonstrate an important role for the properties of neurons within the GPe. In this review, we will discuss these intrinsic GPe properties and review proposed mechanisms for activity decorrelation within the dopamine-intact GPe. Failure of the GPe to desynchronize correlated inputs can be a possible explanation for synchronization in the whole BG. Potential triggers of synchronization involve the enhancement of GPe-GPe inhibition and changes in ion channel function in GPe neurons.
Highlights
Neural activity in the basal ganglia (BG) of patients with idiopathic Parkinson’s disease (PD) and animal models of PD commonly shows high levels of synchronization, bursting, and oscillations in low frequency bands such as θ (4–7 Hz) and β (15–30 Hz) frequencies (Bergman et al, 1994; Obeso et al, 2000; Brown et al, 2001; Montgomery, 2007; Wichmann et al, 2011)
Prominent changes in neural synchronization occur in projection neurons of the GPe, which has a central position in the BG loop (Smith et al, 1998) 1
Despite that in literature the effects of dopamine depletion are often focused on the striatum, PD patients lose about 82% of dopamine in the GPe (Rajput et al, 2008)
Summary
Neural activity in the basal ganglia (BG) of patients with idiopathic Parkinson’s disease (PD) and animal models of PD commonly shows high levels of synchronization, bursting, and oscillations in low frequency bands such as θ (4–7 Hz) and β (15–30 Hz) frequencies (Bergman et al, 1994; Obeso et al, 2000; Brown et al, 2001; Montgomery, 2007; Wichmann et al, 2011). After dopamine depletion, strong synchronization in the β frequency range was found (Nini et al, 1995; Raz et al, 2000; Heimer et al, 2002; Mallet et al, 2008) These findings led to the suggestion of a local mechanism that decorrelates activity in the healthy GPe (BarGad et al, 2003). We describe proposed mechanisms for this synchronization process intrinsic to the GPe, based on synaptic and cellular properties
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