Levodopa gains psychostimulant-like properties after nigral dopaminergic loss.
Identifieur interne : 001100 ( Ncbi/Merge ); précédent : 001099; suivant : 001101Levodopa gains psychostimulant-like properties after nigral dopaminergic loss.
Auteurs : Michel Engeln [France] ; Stefania Fasano ; Serge H. Ahmed ; Martine Cador ; Veerle Baekelandt ; Erwan Bezard ; Pierre-Olivier FernagutSource :
- Annals of neurology [ 1531-8249 ] ; 2013.
English descriptors
- KwdEn :
- Adenoviridae (genetics), Adenoviridae (metabolism), Animals, Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Conditioning, Operant (drug effects), Conditioning, Operant (physiology), Disease Models, Animal, Dopaminergic Neurons (drug effects), Dopaminergic Neurons (pathology), Food Preferences (drug effects), Humans, Levodopa (pharmacology), Levodopa (therapeutic use), Male, Mutation (genetics), Parkinson Disease (drug therapy), Parkinson Disease (etiology), Parkinson Disease (genetics), Parkinson Disease (pathology), Rats, Rats, Wistar, Reward, Saccharin (administration & dosage), Substantia Nigra (pathology), Sweetening Agents (administration & dosage), Taste (drug effects), Transduction, Genetic, Tyrosine 3-Monooxygenase (metabolism), Ubiquitin (metabolism), alpha-Synuclein (genetics), alpha-Synuclein (toxicity).
- MESH :
- chemical , administration & dosage : Saccharin, Sweetening Agents.
- chemical , genetics : alpha-Synuclein.
- chemical , metabolism : Tyrosine 3-Monooxygenase, Ubiquitin.
- chemical , pharmacology : Antiparkinson Agents, Levodopa.
- drug effects : Conditioning, Operant, Dopaminergic Neurons, Food Preferences, Taste.
- drug therapy : Parkinson Disease.
- etiology : Parkinson Disease.
- genetics : Adenoviridae, Mutation, Parkinson Disease.
- metabolism : Adenoviridae.
- pathology : Dopaminergic Neurons, Parkinson Disease, Substantia Nigra.
- physiology : Conditioning, Operant.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- chemical , toxicity : alpha-Synuclein.
- Animals, Disease Models, Animal, Humans, Male, Rats, Rats, Wistar, Reward, Transduction, Genetic.
Abstract
Dopamine dysregulation syndrome shares some core behavioral features with psychostimulant addiction, suggesting that dopamine replacement therapy can acquire psychostimulantlike properties in some patients with Parkinson disease (PD). We here report strong experimental evidence supporting this hypothesis in an α-synuclein rat model of PD. Although levodopa had no effect in controls, it acquired 2 prominent psychostimulantlike properties in Parkinsonian rats: (1) it produced intense reward on its own and in parallel (2) decreased interest in other nondrug reward. These 2 effects may combine to explain the addictive use of levodopa after loss of midbrain dopamine neurons in some PD patients.
DOI: 10.1002/ana.23881
PubMed: 23494678
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 000711
- to stream PubMed, to step Curation: 000680
- to stream PubMed, to step Checkpoint: 000680
Links to Exploration step
pubmed:23494678Le document en format XML
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<front><div type="abstract" xml:lang="en">Dopamine dysregulation syndrome shares some core behavioral features with psychostimulant addiction, suggesting that dopamine replacement therapy can acquire psychostimulantlike properties in some patients with Parkinson disease (PD). We here report strong experimental evidence supporting this hypothesis in an α-synuclein rat model of PD. Although levodopa had no effect in controls, it acquired 2 prominent psychostimulantlike properties in Parkinsonian rats: (1) it produced intense reward on its own and in parallel (2) decreased interest in other nondrug reward. These 2 effects may combine to explain the addictive use of levodopa after loss of midbrain dopamine neurons in some PD patients.</div>
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