L-DOPA-induced dyskinesia: cellular mechanisms and approaches to treatment

被引:38
作者
Cenci, M. Angela [1 ]
机构
[1] Lund Univ, Basal Ganglia Pathophysiol Unit, Dept Expt Med Sci, S-22184 Lund, Sweden
关键词
rodent models; motor complication; dopamine replacement therapy; neuroplasticity;
D O I
10.1016/S1353-8020(08)70014-2
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
L-DOPA-induced dyskinesia (LID) is a common complication of the treatment of Parkinson's disease, and its precise mechanisms have long remained unknown. Rodent models of LID provide a tool to dissect the impact of specific factors on the development and expression of dyskinetic movements. This short review will summarize recent findings from rodent studies that have consolidated and considerably expanded our mechanistic understanding of LID. Based on the experimental findings, the review will propose a chart of possible treatment options acting on different pathophysiological levels. (C) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码:S263 / S267
页数:5
相关论文
共 25 条
[1]   Frequency of levodopa-related dyskinesias and motor fluctuations as estimated from the cumulative literature [J].
Ahlskog, JE ;
Muenter, MD .
MOVEMENT DISORDERS, 2001, 16 (03) :448-458
[2]   Time course of striatal ΔFosB-like immunoreactivity and prodynorphin mRNA levels after discontinuation of chronic dopaminomimetic treatment [J].
Andersson, M ;
Westin, JE ;
Cenci, MA .
EUROPEAN JOURNAL OF NEUROSCIENCE, 2003, 17 (03) :661-666
[3]   Striatal fosB expression is causally linked with L-DOPA-induced abnormal involuntary movements and the associated upregulation of striatal prodynorphin mRNA in a rat model of Parkinson's disease [J].
Andersson, M ;
Hilbertson, A ;
Cenci, MA .
NEUROBIOLOGY OF DISEASE, 1999, 6 (06) :461-474
[4]   cAMP response element-binding protein is required for dopamine-dependent gene expression in the intact but not the dopamine-denervated striatum [J].
Andersson, M ;
Konradi, C ;
Cenci, MA .
JOURNAL OF NEUROSCIENCE, 2001, 21 (24) :9930-9943
[5]   Increased D1 dopamine receptor signaling in levodopa-induced dyskinesia [J].
Aubert, I ;
Guigoni, C ;
Håkansson, K ;
Li, Q ;
Dovero, S ;
Barthe, N ;
Bioulac, BH ;
Gross, CE ;
Fisone, G ;
Bloch, B ;
Bezard, E .
ANNALS OF NEUROLOGY, 2005, 57 (01) :17-26
[6]   PERMANENT HUMAN PARKINSONISM DUE TO 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE (MPTP) - 7 CASES [J].
BALLARD, PA ;
TETRUD, JW ;
LANGSTON, JW .
NEUROLOGY, 1985, 35 (07) :949-956
[7]   Role of striatal L-DOPA in the production of dyskinesia in 6-hydroxydopamine lesioned rats [J].
Carta, M ;
Lindgren, HS ;
Lundblad, M ;
Stancampiano, R ;
Fadda, F ;
Cenci, MA .
JOURNAL OF NEUROCHEMISTRY, 2006, 96 (06) :1718-1727
[8]   Dopamine released from 5-HT terminals is the cause of L-DOPA-induced dyskinesia in Parkinsonian rats [J].
Carta, Manolo ;
Carlsson, Thomas ;
Kirik, Deniz ;
Bjorklund, Anders .
BRAIN, 2007, 130 :1819-1833
[9]   Dopamine dysregulation of movement control in L-DOPA-induced dyskinesia [J].
Cenci, M. Angela .
TRENDS IN NEUROSCIENCES, 2007, 30 (05) :236-243
[10]   Post-versus presynaptic plasticity in L-DOPA-induced dyskinesia [J].
Cenci, M. Angela ;
Lundblad, Martin .
JOURNAL OF NEUROCHEMISTRY, 2006, 99 (02) :381-392