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Cerebral Cortex Advance Access published online on November 7, 2008

Cerebral Cortex, doi:10.1093/cercor/bhn199
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© The Author 2008. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Chronic but not Acute Dopaminergic Transmission Interruption Promotes a Progressive Increase in Cortical Beta Frequency Synchronization: Relationships to Vigilance State and Akinesia

Bertrand Degos1, Jean-Michel Deniau1, Mario Chavez2 and Nicolas Maurice1

1 Institut National de la Santé et de la Recherche Médicale U.667, Dynamique et Physiopathologie des Réseaux Neuronaux, Collège de France, 11 place Marcelin Berthelot, 75 231 Paris Cedex 05, France; Université Pierre et Marie Curie, 4 place Jussieu, 75005 Paris, France, 2 Centre National de la Recherche Scientifique, Unité Propre de Recherche 640 – Laboratoire de Neurosciences Cognitives et Imagerie Cérébrale, Hôpital de la Pitié-Salpêtrière, 75 651 Paris Cedex 13, France

Address correspondence to Nicolas Maurice, INSERM U.667, Collège de France, 11 place Marcelin Berthelot, 75 231 Paris Cedex 05, France. Email: nicolas.maurice{at}college-de-france.fr.

Dopaminergic (DA) denervation results in the appearance of an excessive cortical beta frequency synchronization in parkinsonian patients and animal models of the disease. The present study analyzed electrocorticogram signals in awake rats to further characterize this excessive synchronization in terms of time course, relation to motor activity and state of vigilance. Using substantia nigra pars compacta lesions and both acute and chronic pharmacological interruptions of DA transmission, the present data demonstrated that the appearance of excessive beta synchronization requires a prolonged interruption in DA transmission and builds up progressively. This synchronization was vigilance-state dependent and observed solely during awake-like activity. Furthermore, these data demonstrated for the first time that the appearance of akinesia preceded the excessive cortical beta synchronization. In addition, this synchronization was stronger in the motor than in the somato-sensory cortex and in unilaterally compared with bilaterally lesioned animals. Finally, excessive beta synchronization was accompanied by an increased coherence between motor and somato-sensory cortical activities. These data suggest that excessive beta synchronization is associated with plastic processes whose time course is delayed with respect to the akinesia. Moreover, the expression of this phenomenon, which likely reflects functional changes in the cortico-basal ganglia circuits, requires a specific brain state.

Key Words: basal ganglia • cerebral cortex • EEG • oscillations • Parkinson's disease


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