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Parkinson’s Disease
Volume 2012 (2012), Article ID 358176, 10 pages
Review Article

Corticostriatal Plastic Changes in Experimental L-DOPA-Induced Dyskinesia

1Laboratorio di Neurofisiologia, Fondazione Santa Lucia, IRCCS, Via del Fosso di Fiorano 64, 00143 Rome, Italy
2Clinica Neurologica, Dipartimento Specialità Medico Chirurgiche e Sanità Pubblica, Università di Perugia, S. Maria della Misericordia, 06156 Perugia, Italy

Received 17 January 2012; Accepted 6 March 2012

Academic Editor: Anna Rosa Carta

Copyright © 2012 Veronica Ghiglieri et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


In Parkinson’s disease (PD), alteration of dopamine- (DA-) dependent striatal functions and pulsatile stimulation of DA receptors caused by the discontinuous administration of levodopa (L-DOPA) lead to a complex cascade of events affecting the postsynaptic striatal neurons that might account for the appearance of L-DOPA-induced dyskinesia (LID). Experimental models of LID have been widely used and extensively characterized in rodents and electrophysiological studies provided remarkable insights into the inner mechanisms underlying L-DOPA-induced corticostriatal plastic changes. Here we provide an overview of recent findings that represent a further step into the comprehension of mechanisms underlying maladaptive changes of basal ganglia functions in response to L-DOPA and associated to development of LID.