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J Neurophysiol 102: 1811-1820, 2009. First published July 22, 2009; doi:10.1152/jn.90844.2008
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The Electrocorticogram Signal Can Be Modulated With Deep Brain Stimulation of the Subthalamic Nucleus in the Hemiparkinsonian Rat

M. J. Lehmkuhle1, S. S. Bhangoo2 and D. R. Kipke1

1Department of Biomedical Engineering, University of Michigan, Ann Arbor; and 2Neurosurgery Department, Henry Ford Hospital, Detroit, Michigan

Submitted 1 August 2008; accepted in final form 15 July 2009

Abstract

Electrocorticogram (ECoG) recordings of the 6-hydroxydopamine (6-OHDA)–lesioned parkinsonian rat have shown an increase in the power of cortical β-band (15–30 Hz) oscillations ipsilateral to the lesion. The power of these oscillations is decreased with dopamine agonist administration. Here, we demonstrate that stimulation of an electrode implanted in the subthalamic nucleus alters the power of cortical β and {gamma} oscillations in 6-OHDA–lesioned animals. These alterations are dependent on stimulation frequency, charge, and amplitude/pulse width. Oscillations were significantly reduced during 200- and 350-Hz stimulation. A minimum charge of 4 nC was required to elicit a reduction in oscillation power. A number of amplitude and pulse width combinations that reached 4 nC were tested; it was found that only the combinations of 33 µA/120 µs and 65 µA/60 µs significantly reduced cortical oscillations. The reduction in β/{gamma} oscillation power due to deep brain stimulation (DBS) was consistent with a significant reduction in the animals' rotational behavior, a typical symptom of parkinsonism in the rat. A significant shift from high β to low {gamma} was observed in the peak frequencies of ECoG recordings while animals were at rest versus walking on a treadmill. However, DBS exhibited no differential effect on oscillations between these two states. EEG recordings from rodent models of DBS may provide surrogate information about the neural signatures of Parkinson's disease relative to the efficacy of DBS.


Address for reprint requests and other correspondence: M. J. Lehmkuhle, Physiology Department, University of Utah, 420 Chipeta Way, Suite 1700, Salt Lake City, UT 84132 (E-mail: Mark.Lehmkuhle{at}utah.edu)







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