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New insights into the mechanism of drug-induced dyskinesia

Published online by Cambridge University Press:  20 December 2012

Anton J. M. Loonen  and
Svetlana A. Ivanova
Anton J. M. Loonen*
Affiliation:
Department of Pharmacy, University of Groningen, Groningen, The Netherlands
Svetlana A. Ivanova
Affiliation:
Mental Health Research Institute, Siberian Branch Russian Academy Medical Sciences, Tomsk, Russian Federation
*
*Address for correspondence: Prof. Anton J. M. Loonen, Department of Pharmacy, Antonius Deusinglaan 1, 9713AV Groningen, The Netherlands. (Email a.j.m.loonen@rug.nl)
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Abstract

Dyskinesia is an extrapyramidal movement disorder characterized by involuntary, repetitive, irregular motions that affect the mouth and face and/or the limbs and trunk. Tardive dyskinesia (TD) is a well-known complication of long-term treatment with antipsychotic drugs. Dyskinesia is also induced with levodopa, a treatment for Parkinson's disease, and it occurs spontaneously as a symptom of Huntington's disease. Research on the pathogenesis of TD has focused on a dysfunction of either the dopaminergic or serotonergic system. However, recent evidence has suggested that we should focus on the possible damage of GABAergic medium spiny neurons (MSNs). MSNs are the first station in the cortico-striato-thalamo-cortical circuit that regulates the amplitude and velocity of movements. Two pathways can be distinguished in this circuit: a direct pathway, which increases movements (hyperkinesia), and an indirect pathway, which decreases movements (hypokinesia). Both pathways are activated by glutamatergic corticostriatal neurons. Here, we discuss some evidence that supports the hypothesis that indirect pathway MSNs are damaged in dyskinesia.

Keywords

dyskinesiamechanismlevodopamedium spiny neurons
Type
Opinion
Information
CNS Spectrums , Volume 18 , Issue 1 , February 2013 , pp. 15 - 20
Copyright
Copyright © Cambridge University Press 2012

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