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Cerebral Cortex Advance Access published online on September 11, 2008
Cerebral Cortex, doi:10.1093/cercor/bhn149
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© The Author 2008. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Cortical Effects of Subthalamic Stimulation Correlate with Behavioral Recovery from Dopamine Antagonist Induced Akinesia

Cyril Dejean1, Brian Hyland2 and Gordon Arbuthnott3

1 Departments of Anatomy and Structural Biology, 2 Physiology, University of Otago, Dunedin, New Zealand, 3 Brain Mechanisms for Behaviour Unit, Okinawa Institute for Science and Technology, Okinawa, Japan

Address correspondence to Professor G. W. Arbuthnott, B.Sc., Ph.D. Brain Mechanisms for Behaviour Unit, Okinawa Institute of Science and Technology Promotion Corporation, Initial Research Project, 12-22 Suzaki, Uruma, Okinawa, Japan 904-2234. Email: Gordon{at}oist.jp.

High-frequency stimulation of around 130 Hz delivered to the subthalamic nucleus (STN-DBS [deep brain stimulation]) is an effective treatment of Parkinson's disease (PD), but the mechanisms of its therapeutic effect remain obscure. Recently, it has been shown in anaesthetized rats that STN-DBS antidromically activates cortical neurons with coincident reduction of the cortical slow wave oscillations that occur in this preparation. Here we extend this work; recording the effect of STN-DBS upon cortical EEG and akinesia, in unanesthetized rats rendered cataleptic by acute dopaminergic blockade. STN-DBS–like stimulation resulted in a short latency, presumed antidromic, evoked potential in the cortex. In cataleptic animals, there was a significant increase in the power of beta oscillations in the electroencephalography which was reversed by stimulation that evoked the cortical response. We also observed a significant rescue of motor function, with the level of akinesia (bar test score) being inversely correlated to the amplitude of the evoked potential (R2 = 0.84). These data confirm that (probably antidromic) short latency cortical responses occur in the awake animal and that these are associated with reductions in abnormal cortical oscillations characteristic of PD and with improvements in akinesia. Our results raise the possibility that STN-DBS reduces PD oscillations and symptoms through antidromic cortical activation.

Key Words: antidromic cortical activation • basal ganglia • behavioral recovery • beta band frequencies • dopamine receptor blockers • EEG

Received for publication May 1, 2008. Revision received July 29, 2008. Accepted for publication July 29, 2008.


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