• W Meissner, T Reum, G Paul, D Harnack, R Sohr, R Morgenstern, and A Kupsch.
• Department of Neurology, Charité Campus Virchow-Klinikum, Humboldt-University Berlin, Augustenburger Platz 1, 13353, Berlin, Germany.
• Neurosci. Lett. 2001 May 11;303(3):165-8.

AbstractDeep brain stimulation of the subthalamic nucleus is an established therapeutic strategy for patients with Parkinson's disease. Although the exact mechanisms of action remain unknown, it is noteworthy that dopaminergic medication can be markedly reduced after neurostimulation of the subthalamic nucleus. Previously, we have shown that deep brain stimulation of the subthalamic nucleus is followed by an increase of striatal extracellular dopamine metabolites in naive rats. In the present study we examined the effects of deep brain stimulation on striatal monoamine metabolism in the intrastriatal 6-hydroxydopamine rat model of Parkinson's disease. Deep brain stimulation of the subthalamic nucleus was followed by a delayed increase of extracellular 3,4-dihydroxyphenylacetic and homovanillic whereas dopamine levels were unchanged in stimulated rats and controls. Our results indicate that deep brain stimulation of the subthalamic nucleus affects significantly striatal dopaminergic metabolism in 6-hydroxydopamine lesioned rats.

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