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Previous Article | Next Article
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
Joshua A. Goldberg1, Thomas Boraud1, Sharon Maraton1, Suzanne N. Haber2, Eilon Vaadia1, and Hagai Bergman1 1 Department of Physiology, The Hebrew University-Hadassah Medical School, and the Interdisciplinary Center for Neural Computation, The Hebrew University, Jerusalem 91120, Israel, and 2 Department of Neurobiology and Anatomy, University of Rochester, Rochester, New York 14642
Primary motor cortex (MI) neurons discharge vigorously during voluntary movement. A cardinal symptom of Parkinson's disease (PD) is poverty of movement (akinesia). Current models of PD thus hypothesize that increased inhibitory pallidal output reduces firing rates in frontal cortex, including MI, resulting in akinesia and muscle rigidity. We recorded the simultaneous spontaneous discharge of several neurons in the arm-related area of MI of two monkeys and in the globus pallidus (GP) of one of the two. Accelerometers were fastened to the forelimbs to detect movement, and surface electromyograms were recorded from the contralateral arm of one monkey. The recordings were conducted before and after systemic treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rendering the animals severely akinetic and rigid with little or no tremor. The mean spontaneous MI rates during periods of immobility (four to five spikes/sec) did not change after MPTP; however, in this parkinsonian state, MI neurons discharged in long bursts (sometimes >2 sec long). These bursts were synchronized across many cells but failed to elicit detectable movement, indicating that even robust synchronous MI discharge need not result in movement. These synchronized population bursts were absent from the GP and were on a larger timescale than oscillatory synchrony found in the GP of tremulous MPTP primates, suggesting that MI parkinsonian synchrony arises independently of basal ganglia dynamics. After MPTP, MI neurons responded more vigorously and with less specificity to passive limb movement. Abnormal MI firing patterns and synchronization, rather than reduced firing rates, may underlie PD akinesia and persistent muscle rigidity.
Key words: correlations; neuronal synchronization; EMG; firing patterns; intracortical microstimulation; monkey; striatum; globus pallidus; kinesthetic; oscillations
Copyright © 2002 Society for Neuroscience 0270-6474/02/22114639-15$05.00/0
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