The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Post‐ versus presynaptic plasticity in L‐DOPA‐induced dyskinesia
Open accessAbstract
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.
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Cites
Stages in the development of Parkinson’s disease-related pathology
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A cellular mechanism of reward-related learning
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Loss of bidirectional striatal synaptic plasticity in L-DOPA-induced dyskinesia
Picconi, B., Centonze, D., Håkansson, K., Bernardi, G., Greengard, P., Fisone, G., Cenci, M. A., & Calabresi, P. (2003) · Nature Neuroscience · doi:10.1038/nn1040 · Cited by 821
Self-citationIt could be habit forming: drugs of abuse and striatal synaptic plasticity
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Cited by
Fieblinger, T., Graves, S. M., Sebel, L. E., Alcacer, C., Plotkin, J. L., Gertler, T. S., Chan, C. S., Heiman, M., Greengard, P., Cenci, M. A., et al. (2014) · Nature Communications · doi:10.1038/ncomms6316 · Cited by 295
Self-citationCenci, M. A., & Lundblad, M. (2007) · Current Protocols in Neuroscience · doi:10.1002/0471142301.ns0925s41 · Cited by 266
Self-citationDopamine Gene Therapy for Parkinson’s Disease in a Nonhuman Primate Without Associated Dyskinesia
Jarraya, B., Boulet, S., Scott Ralph, G., Jan, C., Bonvento, G., Azzouz, M., Miskin, J. E., Shin, M., Delzescaux, T., Drouot, X., et al. (2009) · Science Translational Medicine · doi:10.1126/scitranslmed.3000130 · Cited by 186
Nicotine and Parkinson's disease: implications for therapy
Quik, M., O'Leary, K., & Tanner, C. M. (2008) · Movement Disorders · doi:10.1002/mds.21900 · Cited by 154
Nicotine reduces levodopa-induced dyskinesias in lesioned monkeys
Quik, M., Cox, H., Parameswaran, N., O'Leary, K., Langston, J. W., & Di Monte, D. (2007) · Annals of Neurology · doi:10.1002/ana.21203 · Cited by 133
Metadata
- Authors
- Cenci, M. A., & Lundblad, M.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2006-07-26
- Volume
- 99
- Issue
- 2
- Pages
- 381-392
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1973564144
- Cited by
- 218
- References
- 7
- FWCI
- 7.95
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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