Abstract
Movement disorders in Parkinson’s disease (PD) are commonly associated with slow oscillations and increased synchrony of neuronal activity in the basal ganglia. The neural mechanisms underlying this dynamic network dysfunction, however, are only poorly understood. Here, we show that the strength of inhibitory inputs from striatum to globus pallidus external (GPe) is a key parameter controlling oscillations in the basal ganglia. Specifically, the increase in striatal activity observed in PD is sufficient to unleash the oscillations in the basal ganglia. This finding allows us to propose a unified explanation for different phenomena: absence of oscillation in the healthy state of the basal ganglia, oscillations in dopamine-depleted state and quenching of oscillations under deep-brain-stimulation (DBS). These novel insights help us to better understand and optimize the function of DBS protocols. Furthermore, studying the model behavior under transient increase of activity of the striatal neurons projecting to the indirect pathway, we are able to account for both motor impairment in PD patients and for reduced response inhibition in DBS implanted patients.
Highlights
Parkinson’s disease (PD) is a prominent brain disorder, characterized by a host of motor and cognitive dysfunctions, caused by dopamine depletion in the basal ganglia (BG)
The first clue to understand the emergence of oscillations in the basal ganglia system comes from the architecture of the STNGPe network (Figure 1A)
Theoretical and computational work far has focused on the role of increased efficacy of the mutual coupling between Sub-thalamic nucleus (STN) and globus pallidus external (GPe) to explain PD related oscillations in the basal ganglia
Summary
Parkinson’s disease (PD) is a prominent brain disorder, characterized by a host of motor and cognitive dysfunctions, caused by dopamine depletion in the basal ganglia (BG). A distinctive feature of PD is the presence of aberrant oscillations (12–30 Hz, β-band) of the local field potential in the subthalamo-pallidal (STN-GPe) network (Brown and Williams, 2005; Hammond et al, 2007; Eusebio et al, 2008). These oscillations are causally linked to deficits in movement initiation and execution, resting state tremor, and other related symptoms (Tass et al, 2010).
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