Pathogenesis of levodopa-induced dyskinesia: focus on D1 and D3 dopamine receptors.

C. Guigoni, I. Aubert, Q. Li, V.V. Gurevich, J.L. Benovic, S. Ferry, U. Mach, H. Stark, L. Leriche, K. Håkansson, Bernard H. Bioulac, Christian E. Gross, Pierre Sokoloff, Gilberto Fisone, E.V. Gurevich, Bertrand Bloch, Erwan Bezard
Parkinsonism & Related Disorders. 2005-06-01; 11: S25-S29
DOI: 10.1016/j.parkreldis.2004.11.005

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1. Parkinsonism Relat Disord. 2005 Jun;11 Suppl 1:S25-9.

Pathogenesis of levodopa-induced dyskinesia: focus on D1 and D3 dopamine
receptors.

Guigoni C(1), Aubert I, Li Q, Gurevich VV, Benovic JL, Ferry S, Mach U, Stark H,
Leriche L, Håkansson K, Bioulac BH, Gross CE, Sokoloff P, Fisone G, Gurevich EV,
Bloch B, Bezard E.

Author information:
(1)Basal Gang, Laboratoire de Physiologie et Physiopathologie de la Signalisation
Cellulaire, CNRS UMR 5543, Université Victor Segalen-Bordeaux 2, France.

Involuntary movements, or dyskinesia, represent a debilitating complication of
levodopa therapy for Parkinson’s disease. Taking advantage of a monkey brain bank
constituted to study the pathophysiology of levodopa-induced dyskinesia, we here
report the changes affecting D1, D2 and D3 dopamine receptors within the striatum
of four experimental groups of non-human primates: normal, parkinsonian,
parkinsonian treated with levodopa without or with dyskinesia. We also report the
possible role of arrestin and G protein-coupled receptor kinases.

DOI: 10.1016/j.parkreldis.2004.11.005
PMID: 15885624 [Indexed for MEDLINE]


Auteurs Bordeaux Neurocampus