Sparse pallidal connections shape synchrony in a network model of the basal ganglia
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Sparse pallidal connections shape synchrony in a network model of the basal ganglia. / Schwab, Bettina C; van Wezel, Richard J A; van Gils, Stephan A.
In: EUR J NEUROSCI, Vol. 45, No. 8, 04.2017, p. 1000-1012.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Sparse pallidal connections shape synchrony in a network model of the basal ganglia
AU - Schwab, Bettina C
AU - van Wezel, Richard J A
AU - van Gils, Stephan A
N1 - © 2016 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.
PY - 2017/4
Y1 - 2017/4
N2 - Neural synchrony in the basal ganglia, especially in the beta frequency band (13-30 Hz), is a hallmark of Parkinson's disease and considered as antikinetic. In contrast, the healthy basal ganglia show low levels of synchrony. It is currently unknown where synchrony and oscillations arise in the parkinsonian brain and how they are transmitted through the basal ganglia, as well as what makes them dependent on dopamine. The external part of the globus pallidus has recently been identified as a hub nucleus in the basal ganglia, possessing intrinsic inhibitory connections and possibly also gap junctions. In this study, we show that in a conductance-based network model of the basal ganglia, the combination of sparse, high-conductance inhibitory synapses and sparse, low-conductance gap junctions in the external part of the globus pallidus could effectively desynchronize the whole network. However, when gap junction coupling became strong enough, the effect was impeded and activity synchronized. In particular, sustained periods of beta coherence occurred between some neuron pairs. As gap junctions can change their conductance with the dopamine level, we suggest pallidal gap junction coupling as a mechanism contributing to the development of beta synchrony in the parkinsonian basal ganglia.
AB - Neural synchrony in the basal ganglia, especially in the beta frequency band (13-30 Hz), is a hallmark of Parkinson's disease and considered as antikinetic. In contrast, the healthy basal ganglia show low levels of synchrony. It is currently unknown where synchrony and oscillations arise in the parkinsonian brain and how they are transmitted through the basal ganglia, as well as what makes them dependent on dopamine. The external part of the globus pallidus has recently been identified as a hub nucleus in the basal ganglia, possessing intrinsic inhibitory connections and possibly also gap junctions. In this study, we show that in a conductance-based network model of the basal ganglia, the combination of sparse, high-conductance inhibitory synapses and sparse, low-conductance gap junctions in the external part of the globus pallidus could effectively desynchronize the whole network. However, when gap junction coupling became strong enough, the effect was impeded and activity synchronized. In particular, sustained periods of beta coherence occurred between some neuron pairs. As gap junctions can change their conductance with the dopamine level, we suggest pallidal gap junction coupling as a mechanism contributing to the development of beta synchrony in the parkinsonian basal ganglia.
KW - Algorithms
KW - Animals
KW - Basal Ganglia/physiology
KW - Beta Rhythm/physiology
KW - Computer Simulation
KW - Cortical Synchronization/physiology
KW - Dopamine/metabolism
KW - Gap Junctions/metabolism
KW - Humans
KW - Models, Neurological
KW - Neural Inhibition/physiology
KW - Neural Pathways/physiology
KW - Neurons/physiology
KW - Rats
KW - Software
U2 - 10.1111/ejn.13324
DO - 10.1111/ejn.13324
M3 - SCORING: Journal article
C2 - 27350120
VL - 45
SP - 1000
EP - 1012
JO - EUR J NEUROSCI
JF - EUR J NEUROSCI
SN - 0953-816X
IS - 8
ER -
