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- M. M. McCarthy
- Department of Mathematics and Statistics, Boston University, Boston, MA 02215;
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- C. Moore-Kochlacs
- Department of Mathematics and Statistics, Boston University, Boston, MA 02215;
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- X. Gu
- Department of Biomedical Engineering, Photonics Center, Boston University, Boston, MA 02215; and
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- E. S. Boyden
- Media Lab, Massachusetts Institute of Technology, Cambridge, MA 02139
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- X. Han
- Department of Biomedical Engineering, Photonics Center, Boston University, Boston, MA 02215; and
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- N. Kopell
- Department of Mathematics and Statistics, Boston University, Boston, MA 02215;
説明
<jats:p>Enhanced oscillations at beta frequencies (8–30 Hz) are a signature neural dynamic pathology in the basal ganglia and cortex of Parkinson's disease patients. The mechanisms underlying these pathological beta oscillations remain elusive. Here, using mathematical models, we find that robust beta oscillations can emerge from inhibitory interactions between striatal medium spiny neurons. The interaction of the synaptic GABAa currents and the intrinsic membrane M-current promotes population oscillations in the beta frequency range. Increased levels of cholinergic drive, a condition relevant to the parkinsonian striatum, lead to enhanced beta oscillations in the striatal model. We show experimentally that direct infusion of the cholinergic agonist carbachol into the striatum, but not into the neighboring cortex, of the awake, normal rodent induces prominent beta frequency oscillations in the local field potential. These results provide evidence for amplification of normal striatal network dynamics as a mechanism responsible for the enhanced beta frequency oscillations in Parkinson's disease.</jats:p>
収録刊行物
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- Proceedings of the National Academy of Sciences
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Proceedings of the National Academy of Sciences 108 (28), 11620-11625, 2011-06-22
Proceedings of the National Academy of Sciences
