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Post- versus presynaptic plasticity in L-DOPA-induced dyskinesia.
J Neurochem. 2006 Oct; 99(2):381-92.JN

Abstract

L-3,4-dihydroxyphenylalanine (L-DOPA) remains the most efficacious drug for the treatment of Parkinson's disease (PD), but causes adverse effects that limit its utility. L-DOPA-induced dyskinesia (abnormal involuntary movements) is a significant clinical problem that attracts growing scientific interest. Current notions attribute the development of dyskinesia to two main factors, viz. the loss of nigrostriatal dopamine (DA) projections and the maladaptive changes produced by L-DOPA at sites postsynaptic to the nigrostriatal neuron. Basic research in the past 15 years has placed a lot of emphasis on the postsynaptic plasticity associated with dyskinesia, but recent experimental work shows that also some presynaptic factors, involving the regulation of L-DOPA/DA release and metabolism in the brain, may show plasticity during treatment. This review summarizes significant studies of L-DOPA-induced dyskinesia in patients and animal models, and outlines directions for future experiments addressing mechanisms of presynaptic plasticity. These investigations may uncover clues to the varying susceptibility to L-DOPA-induced dyskinesia among PD patients, paving the way for tailor-made treatments.

Authors+Show Affiliations

Department of Experimental Medical Science, Basal Ganglia Pathophysiology Unit, Lund University, BMC F11, S.221 84 Lund, Sweden. Angela.Cenci_Nilsson@med.lu.seNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

16942598

Citation

Cenci, M Angela, and Martin Lundblad. "Post- Versus Presynaptic Plasticity in L-DOPA-induced Dyskinesia." Journal of Neurochemistry, vol. 99, no. 2, 2006, pp. 381-92.
Cenci MA, Lundblad M. Post- versus presynaptic plasticity in L-DOPA-induced dyskinesia. J Neurochem. 2006;99(2):381-92.
Cenci, M. A., & Lundblad, M. (2006). Post- versus presynaptic plasticity in L-DOPA-induced dyskinesia. Journal of Neurochemistry, 99(2), 381-92.
Cenci MA, Lundblad M. Post- Versus Presynaptic Plasticity in L-DOPA-induced Dyskinesia. J Neurochem. 2006;99(2):381-92. PubMed PMID: 16942598.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Post- versus presynaptic plasticity in L-DOPA-induced dyskinesia. AU - Cenci,M Angela, AU - Lundblad,Martin, Y1 - 2006/08/29/ PY - 2006/9/1/pubmed PY - 2007/1/9/medline PY - 2006/9/1/entrez SP - 381 EP - 92 JF - Journal of neurochemistry JO - J Neurochem VL - 99 IS - 2 N2 - L-3,4-dihydroxyphenylalanine (L-DOPA) remains the most efficacious drug for the treatment of Parkinson's disease (PD), but causes adverse effects that limit its utility. L-DOPA-induced dyskinesia (abnormal involuntary movements) is a significant clinical problem that attracts growing scientific interest. Current notions attribute the development of dyskinesia to two main factors, viz. the loss of nigrostriatal dopamine (DA) projections and the maladaptive changes produced by L-DOPA at sites postsynaptic to the nigrostriatal neuron. Basic research in the past 15 years has placed a lot of emphasis on the postsynaptic plasticity associated with dyskinesia, but recent experimental work shows that also some presynaptic factors, involving the regulation of L-DOPA/DA release and metabolism in the brain, may show plasticity during treatment. This review summarizes significant studies of L-DOPA-induced dyskinesia in patients and animal models, and outlines directions for future experiments addressing mechanisms of presynaptic plasticity. These investigations may uncover clues to the varying susceptibility to L-DOPA-induced dyskinesia among PD patients, paving the way for tailor-made treatments. SN - 0022-3042 UR - https://www.unboundmedicine.com/medline/citation/16942598/Post__versus_presynaptic_plasticity_in_L_DOPA_induced_dyskinesia_ L2 - https://doi.org/10.1111/j.1471-4159.2006.04124.x DB - PRIME DP - Unbound Medicine ER -