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Enhanced Synchrony among Primary Motor Cortex Neurons in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Primate Model of Parkinson's Disease

Enhanced Synchrony among Primary Motor Cortex Neurons in the... The Journal of Neuroscience, June 1, 2002, 22(11):4639–4653 Enhanced Synchrony among Primary Motor Cortex Neurons in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Primate Model of Parkinson’s Disease 1 1 1 2 1 Joshua A. Goldberg, Thomas Boraud, Sharon Maraton, Suzanne N. Haber, Eilon Vaadia, and Hagai Bergman Department of Physiology, The Hebrew University–Hadassah Medical School, and the Interdisciplinary Center for Neural Computation, The Hebrew University, Jerusalem 91120, Israel, and Department of Neurobiology and Anatomy, University of Rochester, Rochester, New York 14642 Primary motor cortex (MI) neurons discharge vigorously during however, in this parkinsonian state, MI neurons discharged in voluntary movement. A cardinal symptom of Parkinson’s dis- long bursts (sometimes 2 sec long). These bursts were syn- ease (PD) is poverty of movement (akinesia). Current models of chronized across many cells but failed to elicit detectable PD thus hypothesize that increased inhibitory pallidal output movement, indicating that even robust synchronous MI dis- reduces firing rates in frontal cortex, including MI, resulting in charge need not result in movement. These synchronized pop- akinesia and muscle rigidity. We recorded the simultaneous ulation bursts were absent from the GP and were on a larger spontaneous discharge of several neurons in the arm-related timescale than oscillatory synchrony found http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neuroscience Unpaywall

Enhanced Synchrony among Primary Motor Cortex Neurons in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Primate Model of Parkinson's Disease

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Unpaywall
ISSN
0270-6474
DOI
10.1523/jneurosci.22-11-04639.2002
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Abstract

The Journal of Neuroscience, June 1, 2002, 22(11):4639–4653 Enhanced Synchrony among Primary Motor Cortex Neurons in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Primate Model of Parkinson’s Disease 1 1 1 2 1 Joshua A. Goldberg, Thomas Boraud, Sharon Maraton, Suzanne N. Haber, Eilon Vaadia, and Hagai Bergman Department of Physiology, The Hebrew University–Hadassah Medical School, and the Interdisciplinary Center for Neural Computation, The Hebrew University, Jerusalem 91120, Israel, and Department of Neurobiology and Anatomy, University of Rochester, Rochester, New York 14642 Primary motor cortex (MI) neurons discharge vigorously during however, in this parkinsonian state, MI neurons discharged in voluntary movement. A cardinal symptom of Parkinson’s dis- long bursts (sometimes 2 sec long). These bursts were syn- ease (PD) is poverty of movement (akinesia). Current models of chronized across many cells but failed to elicit detectable PD thus hypothesize that increased inhibitory pallidal output movement, indicating that even robust synchronous MI dis- reduces firing rates in frontal cortex, including MI, resulting in charge need not result in movement. These synchronized pop- akinesia and muscle rigidity. We recorded the simultaneous ulation bursts were absent from the GP and were on a larger spontaneous discharge of several neurons in the arm-related timescale than oscillatory synchrony found

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Journal of Neuroscience – Unpaywall

Published: Jun 1, 2002

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