Levodopa gains psychostimulant‐like properties after nigral dopaminergic loss
Identifieur interne : 000E64 ( Main/Exploration ); précédent : 000E63; suivant : 000E65Levodopa gains psychostimulant‐like properties after nigral dopaminergic loss
Auteurs : Michel Engeln [France] ; Stefania Fasano [Italie] ; Serge H. Ahmed [France] ; Martine Cador [France] ; Veerle Baekelandt [Belgique] ; Erwan Bezard [France] ; Pierre-Olivier Fernagut [France]Source :
- Annals of Neurology [ 0364-5134 ] ; 2013-07.
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. Ann Neurol 2013;74:140–144
Url:
- https://api.istex.fr/document/83FE1078C36E1437D794AE68D5AEC6C76421ABFC/fulltext/pdf
- https://hal.archives-ouvertes.fr/hal-01153692
DOI: 10.1002/ana.23881
Affiliations:
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Le document en format XML
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<term>Antiparkinson Agents (therapeutic use)</term>
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<term>Conditioning, Operant (physiology)</term>
<term>Disease Models, Animal</term>
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<term>Dopaminergic Neurons (pathology)</term>
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<term>Levodopa (therapeutic use)</term>
<term>Male</term>
<term>Mutation (genetics)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (etiology)</term>
<term>Parkinson Disease (genetics)</term>
<term>Parkinson Disease (pathology)</term>
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<term>Rats, Wistar</term>
<term>Reward</term>
<term>Saccharin (administration & dosage)</term>
<term>Substantia Nigra (pathology)</term>
<term>Sweetening Agents (administration & dosage)</term>
<term>Taste (drug effects)</term>
<term>Transduction, Genetic</term>
<term>Tyrosine 3-Monooxygenase (metabolism)</term>
<term>Ubiquitin (metabolism)</term>
<term>alpha-Synuclein (genetics)</term>
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<front><div type="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. Ann Neurol 2013;74:140–144</div>
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