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2015 ; 11
(12
): e1004609
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Computational Models Describing Possible Mechanisms for Generation of Excessive
Beta Oscillations in Parkinson s Disease
#MMPMID26683341
Pavlides A
; Hogan SJ
; Bogacz R
PLoS Comput Biol
2015[Dec]; 11
(12
): e1004609
PMID26683341
show ga
In Parkinson's disease, an increase in beta oscillations within the basal ganglia
nuclei has been shown to be associated with difficulty in movement initiation. An
important role in the generation of these oscillations is thought to be played by
the motor cortex and by a network composed of the subthalamic nucleus (STN) and
the external segment of globus pallidus (GPe). Several alternative models have
been proposed to describe the mechanisms for generation of the Parkinsonian beta
oscillations. However, a recent experimental study of Tachibana and colleagues
yielded results which are challenging for all published computational models of
beta generation. That study investigated how the presence of beta oscillations in
a primate model of Parkinson's disease is affected by blocking different
connections of the STN-GPe circuit. Due to a large number of experimental
conditions, the study provides strong constraints that any mechanistic model of
beta generation should satisfy. In this paper we present two models consistent
with the data of Tachibana et al. The first model assumes that Parkinsonian beta
oscillation are generated in the cortex and the STN-GPe circuits resonates at
this frequency. The second model additionally assumes that the feedback from
STN-GPe circuit to cortex is important for maintaining the oscillations in the
network. Predictions are made about experimental evidence that is required to
differentiate between the two models, both of which are able to reproduce firing
rates, oscillation frequency and effects of lesions carried out by Tachibana and
colleagues. Furthermore, an analysis of the models reveals how the amplitude and
frequency of the generated oscillations depend on parameters.