Advances in understanding l-DOPA-induced dyskinesia.
(2007) In Current Opinion in Neurobiology 17(6). p.665-671- Abstract
- The crucial role of dopamine (DA) in movement control is illustrated by the spectrum of motor disorders caused by either a deficiency or a hyperactivity of dopaminergic transmission in the basal ganglia. The degeneration of nigrostriatal DA neurons in Parkinson's disease causes poverty and slowness of movement. These symptoms are greatly improved by pharmacological DA replacement with l-3,4-dihydroxy-phenylalanine (l-DOPA), which however causes excessive involuntary movements in a majority of patients. l-DOPA-induced dyskinesia (abnormal involuntary movements) provides a topic of investigation at the interface between clinical and basic neuroscience. In this article, we review recent studies in rodent models, which have uncovered two... (More)
- The crucial role of dopamine (DA) in movement control is illustrated by the spectrum of motor disorders caused by either a deficiency or a hyperactivity of dopaminergic transmission in the basal ganglia. The degeneration of nigrostriatal DA neurons in Parkinson's disease causes poverty and slowness of movement. These symptoms are greatly improved by pharmacological DA replacement with l-3,4-dihydroxy-phenylalanine (l-DOPA), which however causes excessive involuntary movements in a majority of patients. l-DOPA-induced dyskinesia (abnormal involuntary movements) provides a topic of investigation at the interface between clinical and basic neuroscience. In this article, we review recent studies in rodent models, which have uncovered two principal alterations at the basis of the movement disorder, namely, an abnormal pre-synaptic handling of exogenous l-DOPA, and a hyper-reactive post-synaptic response to DA. Dysregulated nigrostriatal DA transmission causes secondary alterations in a variety of non-dopaminergic transmitter systems, the manipulation of which modulates dyskinesia through mechanisms that are presently unclear. Further research on l-DOPA-induced dyskinesia will contribute to a deeper understanding of the functional interplay between neurotransmitters and neuromodulators in the motor circuits of the basal ganglia. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1052974
- author
- Cenci Nilsson, Angela LU and Lindgren, Hanna LU
- organization
- publishing date
- 2007
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Current Opinion in Neurobiology
- volume
- 17
- issue
- 6
- pages
- 665 - 671
- publisher
- Elsevier
- external identifiers
-
- pmid:18308560
- wos:000255181100008
- scopus:40749157838
- pmid:18308560
- ISSN
- 1873-6882
- DOI
- 10.1016/j.conb.2008.01.004
- language
- English
- LU publication?
- yes
- id
- beaf2cdc-ca4b-4f42-ad1b-f7962985bc20 (old id 1052974)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/18308560?dopt=Abstract
- date added to LUP
- 2016-04-04 07:57:40
- date last changed
- 2022-02-05 23:17:05
@article{beaf2cdc-ca4b-4f42-ad1b-f7962985bc20, abstract = {{The crucial role of dopamine (DA) in movement control is illustrated by the spectrum of motor disorders caused by either a deficiency or a hyperactivity of dopaminergic transmission in the basal ganglia. The degeneration of nigrostriatal DA neurons in Parkinson's disease causes poverty and slowness of movement. These symptoms are greatly improved by pharmacological DA replacement with l-3,4-dihydroxy-phenylalanine (l-DOPA), which however causes excessive involuntary movements in a majority of patients. l-DOPA-induced dyskinesia (abnormal involuntary movements) provides a topic of investigation at the interface between clinical and basic neuroscience. In this article, we review recent studies in rodent models, which have uncovered two principal alterations at the basis of the movement disorder, namely, an abnormal pre-synaptic handling of exogenous l-DOPA, and a hyper-reactive post-synaptic response to DA. Dysregulated nigrostriatal DA transmission causes secondary alterations in a variety of non-dopaminergic transmitter systems, the manipulation of which modulates dyskinesia through mechanisms that are presently unclear. Further research on l-DOPA-induced dyskinesia will contribute to a deeper understanding of the functional interplay between neurotransmitters and neuromodulators in the motor circuits of the basal ganglia.}}, author = {{Cenci Nilsson, Angela and Lindgren, Hanna}}, issn = {{1873-6882}}, language = {{eng}}, number = {{6}}, pages = {{665--671}}, publisher = {{Elsevier}}, series = {{Current Opinion in Neurobiology}}, title = {{Advances in understanding l-DOPA-induced dyskinesia.}}, url = {{http://dx.doi.org/10.1016/j.conb.2008.01.004}}, doi = {{10.1016/j.conb.2008.01.004}}, volume = {{17}}, year = {{2007}}, }