Aberrant striatal plasticity is specifically associated with dyskinesia following levodopa treatment
Identifieur interne : 001E74 ( Main/Exploration ); précédent : 001E73; suivant : 001E75Aberrant striatal plasticity is specifically associated with dyskinesia following levodopa treatment
Auteurs : Pauline Belujon [États-Unis] ; Daniel J. Lodge [États-Unis] ; Anthony A. Grace [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2010-08-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Action Potentials (drug effects), Action Potentials (physiology), Animals, Antiparkinson Agents (adverse effects), Behavior, Animal (drug effects), Cholera Toxin (metabolism), Corpus Striatum (cytology), Corpus Striatum (drug effects), Corpus Striatum (physiopathology), Disease Models, Animal, Dyskinesia, Dyskinesia, Drug-Induced (etiology), Dyskinesia, Drug-Induced (pathology), Dyskinesia, Drug-Induced (physiopathology), Fluorescent Dyes (metabolism), Levodopa, Levodopa (adverse effects), Long-Term Potentiation (drug effects), Long-Term Potentiation (physiology), Nervous system diseases, Neuronal Plasticity (drug effects), Neuronal Plasticity (physiology), Neurons (drug effects), Neurons (metabolism), Neurons (pathology), Neurons (physiology), Oxidopamine (toxicity), Parkinson Disease (drug therapy), Parkinson Disease (etiology), Parkinson's disease, Plasticity, Rats, Substantia Nigra (drug effects), Substantia Nigra (physiopathology), Treatment, Tyrosine 3-Monooxygenase (metabolism), basal ganglia, dopamine, motor cortex, synaptic plasticity.
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- cytology : Corpus Striatum.
- drug effects : Action Potentials, Behavior, Animal, Corpus Striatum, Long-Term Potentiation, Neuronal Plasticity, Neurons, Substantia Nigra.
- drug therapy : Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced, Parkinson Disease.
- chemical , metabolism : Cholera Toxin, Fluorescent Dyes, Neurons, Tyrosine 3-Monooxygenase.
- pathology : Dyskinesia, Drug-Induced, Neurons.
- physiology : Action Potentials, Long-Term Potentiation, Neuronal Plasticity, Neurons.
- physiopathology : Corpus Striatum, Dyskinesia, Drug-Induced, Substantia Nigra.
- chemical , toxicity : Oxidopamine.
- Animals, Disease Models, Animal, Rats.
Abstract
Chronic levodopa treatment for Parkinson's disease often results in the development of abnormal involuntary movement, known as L‐dopa‐induced dyskinesia (LIDs). Studies suggest that LIDs may be associated with aberrant corticostriatal plasticity. Using in vivo extracellular recordings from identified Type I and Type II medium spiny striatal neurons, chronic L‐dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic L‐dopa treatment in dopamine‐depleted rats, there was a transition from a cortically evoked long‐term depression (LTD) to a complementary but opposing form of plasticity, long‐term potentiation, in Type II “indirect” pathway neurons. In contrast, LTD could still be induced in Type I neurons. Interestingly, the one parameter that correlated best with dyskinesias was the inability to de‐depress established LTD in Type I medium spiny striatal neurons. Taken as a whole, we propose that the induction of LIDs is due, at least in part, to an aberrant induction of plasticity within the Type II indirect pathway neurons combined with an inability to de‐depress established plastic responses in Type I neurons. Such information is critical for understanding the cellular mechanisms underlying one of the major caveats to L‐dopa therapy. © 2010 Movement Disorder Society
Url:
- https://api.istex.fr/document/DB8EDA6676CB1F8C57A2E09D1FD030B4322EF91D/fulltext/pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3224800
DOI: 10.1002/mds.23245
Affiliations:
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Le document en format XML
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Studies suggest that LIDs may be associated with aberrant corticostriatal plasticity. Using in vivo extracellular recordings from identified Type I and Type II medium spiny striatal neurons, chronic L‐dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic L‐dopa treatment in dopamine‐depleted rats, there was a transition from a cortically evoked long‐term depression (LTD) to a complementary but opposing form of plasticity, long‐term potentiation, in Type II “indirect” pathway neurons. In contrast, LTD could still be induced in Type I neurons. Interestingly, the one parameter that correlated best with dyskinesias was the inability to de‐depress established LTD in Type I medium spiny striatal neurons. Taken as a whole, we propose that the induction of LIDs is due, at least in part, to an aberrant induction of plasticity within the Type II indirect pathway neurons combined with an inability to de‐depress established plastic responses in Type I neurons. Such information is critical for understanding the cellular mechanisms underlying one of the major caveats to L‐dopa therapy. © 2010 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Pennsylvanie</li><li>Texas</li></region><settlement><li>Pittsburgh</li></settlement><orgName><li>Université de Pittsburgh</li></orgName></list><tree><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Belujon, Pauline" sort="Belujon, Pauline" uniqKey="Belujon P" first="Pauline" last="Belujon">Pauline Belujon</name></region><name sortKey="Grace, Anthony A" sort="Grace, Anthony A" uniqKey="Grace A" first="Anthony A." last="Grace">Anthony A. Grace</name><name sortKey="Lodge, Daniel J" sort="Lodge, Daniel J" uniqKey="Lodge D" first="Daniel J." last="Lodge">Daniel J. Lodge</name><name sortKey="Lodge, Daniel J" sort="Lodge, Daniel J" uniqKey="Lodge D" first="Daniel J." last="Lodge">Daniel J. Lodge</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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