Presynaptic effects of levodopa and their possible role in dyskinesia.
Identifieur interne : 000109 ( Main/Exploration ); précédent : 000108; suivant : 000110Presynaptic effects of levodopa and their possible role in dyskinesia.
Auteurs : Eugene V. Mosharov [États-Unis] ; Anders Borgkvist ; David SulzerSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2015.
English descriptors
- KwdEn :
- Animals, Dopamine (metabolism), Dopamine Agents (adverse effects), Dyskinesia, Drug-Induced (etiology), Dyskinesia, Drug-Induced (metabolism), Dyskinesia, Drug-Induced (pathology), Humans, Levodopa (adverse effects), Neurons (cytology), Neurons (drug effects), Parkinson Disease (drug therapy), Presynaptic Terminals (drug effects), Presynaptic Terminals (metabolism).
- MESH :
- chemical , adverse effects : Dopamine Agents, Levodopa.
- chemical , metabolism : Dopamine.
- cytology : Neurons.
- drug effects : Neurons, Presynaptic Terminals.
- drug therapy : Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced.
- metabolism : Dyskinesia, Drug-Induced, Presynaptic Terminals.
- pathology : Dyskinesia, Drug-Induced.
- Animals, Humans.
Abstract
Levodopa replacement therapy has long provided the most effective treatment for Parkinson's disease (PD). We review how this dopamine (DA) precursor enhances dopaminergic transmission by providing a greater sphere of neurotransmitter influence as a result of the confluence of increased quantal size and decreased DA reuptake, as well as loading DA as a false transmitter into surviving serotonin neuron synaptic vesicles. We further review literature on how presynaptic dysregulation of DA release after l-dopa might trigger dyskinesias in PD patients.
DOI: 10.1002/mds.26103
PubMed: 25450307
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Levodopa replacement therapy has long provided the most effective treatment for Parkinson's disease (PD). We review how this dopamine (DA) precursor enhances dopaminergic transmission by providing a greater sphere of neurotransmitter influence as a result of the confluence of increased quantal size and decreased DA reuptake, as well as loading DA as a false transmitter into surviving serotonin neuron synaptic vesicles. We further review literature on how presynaptic dysregulation of DA release after l-dopa might trigger dyskinesias in PD patients.</div>
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<country name="États-Unis"><region name="État de New York"><name sortKey="Mosharov, Eugene V" sort="Mosharov, Eugene V" uniqKey="Mosharov E" first="Eugene V" last="Mosharov">Eugene V. Mosharov</name>
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