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. 2013 Sep 5;7:124.
doi: 10.3389/fncom.2013.00124. eCollection 2013.

Basal Ganglia Modulation of Thalamocortical Relay in Parkinson's Disease and Dystonia

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Free PMC article

Basal Ganglia Modulation of Thalamocortical Relay in Parkinson's Disease and Dystonia

Yixin Guo et al. Front Comput Neurosci. .
Free PMC article

Abstract

Basal ganglia dysfunction has being implied in both Parkinson's disease and dystonia. While these disorders probably involve different cellular and circuit pathologies within and beyond basal ganglia, there may be some shared neurophysiological pathways. For example, pallidotomy and pallidal Deep Brain Stimulation (DBS) are used in symptomatic treatment of both disorders. Both conditions are marked by alterations of rhythmicity of neural activity throughout basal ganglia-thalamocortical circuits. Increased synchronized oscillatory activity in beta band is characteristic of Parkinson's disease, while different frequency bands, theta and alpha, are involved in dystonia. We compare the effect of the activity of GPi, the output nuclei of the basal ganglia, on information processing in the downstream neural circuits of thalamus in Parkinson's disease and dystonia. We use a data-driven computational approach, a computational model of the thalamocortical (TC) cell modulated by experimentally recorded data, to study the differences and similarities of thalamic dynamics in dystonia and Parkinson's disease. Our analysis shows no substantial differences in TC relay between the two conditions. Our results suggest that, similar to Parkinson's disease, a disruption of thalamic processing could also be involved in dystonia. Moreover, the degree to which TC relay fidelity is impaired is approximately the same in both conditions. While Parkinson's disease and dystonia may have different pathologies and differ in the oscillatory content of neural discharge, our results suggest that the effect of patterning of pallidal discharge is similar in both conditions. Furthermore, these results suggest that the mechanisms of GPi DBS in dystonia may involve improvement of TC relay fidelity.

Keywords: Parkinson's disease; basal ganglia; dystonia; globus pallidus; thalamocortical relay.

Figures

Figure 1
Figure 1
Example of TC relay of periodic excitatory inputs to thalamus under pallidal inhibition in a parkinsonian (A,B) and dystonic (C,D) patients. Upper traces in (A,C) are inhibitory synaptic input from GPi, middle traces are the activity of TC cells, bottom traces are excitatory synaptic input to TC cells. A rectangular box in (A) marks bad TC relay responses, rectangular box in (C) marks miss TC responses. (B,D) are the normalized histograms of the averaged synaptic input from pallidum to thalamus s as defined by Equation (3) (see Averaged GPi synaptic input to TC in Methods for the details). They show the probability that the value of s falls into the bins centered from 0.1 up to 0.8 with 0.1 increments. Synaptic input is high during elevated spiking episodes and low in between them, so that bimodal distribution points to the presence of bursting-like activity. The histograms are for one full episode of recording data from these patients.
Figure 2
Figure 2
Indices of fidelity of thalamocortical relay for parkinsonian patients. Indices for non-transmitted spikes (miss indices) are at subplots (A,C); indices for extra spikes (bad indices) are at subplots (B,D). Periodic excitatory spike train to thalamocortical relay cell are at (A,B); random excitation to thalamocortical relay cell are at (C,D). The indices are plotted against EST (elevated spike time, the fraction of elevated spiking episodes over the total simulation time) and CST (contributed silent time, the fraction of all contributed silent episodes during the simulation time), see Methods.
Figure 3
Figure 3
Indices of fidelity of thalamocortical relay for dystonic patients. Indices for non-transmitted spikes (miss indices) are at subplots (A,C); indices for extra spikes (bad indices) are at subplots (B,D). Periodic excitatory spike train to thalamocortical relay cell are at (A,B); random excitation to thalamocortical relay cell are at (C,D). The indices are plotted against EST (elevated spike time, the fraction of elevated spiking episodes over the total simulation time) and CST (contributed silent time, the fraction of all contributed silent episodes during the simulation time), see Methods.
Figure 4
Figure 4
The distributions of EST (A,C) and CST (B,D) for parkinsonian (A,B) and dystonic (C,D) data.
Figure 5
Figure 5
The distributions of the averaged synaptic input from pallidum to thalamus s [as defined by Equation (3)] for parkinsonian (A) and dystonic (B) data. These figures are similar to Figures 1B,D, but are computed from all the data used in this study.
Figure 6
Figure 6
The relay error indices for parkinsonian and dystonic patients: bad index, the fraction of additional spikes (A), miss index, the fraction of non-transmitted spikes (B), and error index, the sum of the first two (C). The bars indicate mean values, the lines indicate standard deviations. Gray bars indicate periodic excitatory input, white bars indicate random excitatory input. Left pair of bars in each subplot is obtained from dystonic patients data, right pair of bars come from parkinsonian data.

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