MovDisordV3, PascalFrancis, Corpus, bibRecord, 002631

The monoamine reuptake blocker brasofensine reverses akinesia without dyskinesia in MPTP-treated and levodopa-primed common marmosets

Identifieur interne : 002631 ( PascalFrancis/Corpus ); précédent : 002630; suivant : 002632

The monoamine reuptake blocker brasofensine reverses akinesia without dyskinesia in MPTP-treated and levodopa-primed common marmosets

Auteurs : Ronald K. B. Pearce ; Lance A. Smith ; Michael J. Jackson ; Tara Banerji ; Jorgen Scheel-Krüger ; Peter Jenner

Source :

Movement disorders [ 0885-3185 ] ; 2002.

RBID : Pascal:02-0584250

Descripteurs français

Pascal (Inist)
- Parkinson maladie, Dyskinésie, Brasofensine, Inhibiteur recapture, Dopamine, Antiparkinsonien, Pathologie expérimentale, Traitement, Animal, Singe, Chimiothérapie.

English descriptors

KwdEn :
- Animal, Antiparkinson agent, Brasofensine, Chemotherapy, Dopamine, Dyskinesia, Experimental disease, Monkey, Parkinson disease, Reuptake inhibitor, Treatment.

Abstract

The common marmoset develops motor deficits after MPTP treatment and exhibits dyskinesia after chronic levodopa (L-dopa) dosing and subsequent re-challenge with L-dopa and other dopaminergic agents. We report on the actions of the potent monoamine reuptake blocker brasofensine on motor disability, locomotor activity, and dyskinesia in the 1-methyl-4-1, 2,3,6-tetrahydropyridine (MPTP) -treated marmoset model of Parkinson's disease. Oral administration of brasofensine (0.25, 0.5, 1.0, or 2.5 mg/kg) to MPTP-treated marmosets produced a long-lasting, dose-dependent increase in locomotor activity and reduction in disability scores. In addition, coadministration of the lowest dose of brasofensine (0.25 mg/kg orally) with a threshold oral dose of L-dopa (2.5 mg/kg) caused a marked increase in locomotor activity, greater than that produced by either drug alone. In other MPTP-treated marmosets previously primed to exhibit dyskinesia by repeated L-dopa dosing, brasofensine effectively reversed akinesia with a naturalistic and prolonged motor response without the appearance of dyskinesia or stereotypy. This finding contrasts with the severe dyskinesia, stereotypy, and hyperkinesis produced by equivalent doses of L-dopa. The ability of brasofensine to produce a prolonged and naturalistic antiparkinsonian response without eliciting dyskinesia after previous L-dopa priming may relate to actions on D₁ receptor-linked pathways. These findings suggest that monoamine reuptake blockade may be of value in the treatment of Parkinson's disease, both early in the disease course and when L-dopa-induced dyskinesias complicate treatment.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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C01	`01`		`ENG`	@0 The common marmoset develops motor deficits after MPTP treatment and exhibits dyskinesia after chronic levodopa (L-dopa) dosing and subsequent re-challenge with L-dopa and other dopaminergic agents. We report on the actions of the potent monoamine reuptake blocker brasofensine on motor disability, locomotor activity, and dyskinesia in the 1-methyl-4-1, 2,3,6-tetrahydropyridine (MPTP) -treated marmoset model of Parkinson's disease. Oral administration of brasofensine (0.25, 0.5, 1.0, or 2.5 mg/kg) to MPTP-treated marmosets produced a long-lasting, dose-dependent increase in locomotor activity and reduction in disability scores. In addition, coadministration of the lowest dose of brasofensine (0.25 mg/kg orally) with a threshold oral dose of L-dopa (2.5 mg/kg) caused a marked increase in locomotor activity, greater than that produced by either drug alone. In other MPTP-treated marmosets previously primed to exhibit dyskinesia by repeated L-dopa dosing, brasofensine effectively reversed akinesia with a naturalistic and prolonged motor response without the appearance of dyskinesia or stereotypy. This finding contrasts with the severe dyskinesia, stereotypy, and hyperkinesis produced by equivalent doses of L-dopa. The ability of brasofensine to produce a prolonged and naturalistic antiparkinsonian response without eliciting dyskinesia after previous L-dopa priming may relate to actions on D₁ receptor-linked pathways. These findings suggest that monoamine reuptake blockade may be of value in the treatment of Parkinson's disease, both early in the disease course and when L-dopa-induced dyskinesias complicate treatment.
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Format Inist (serveur)

NO :	PASCAL 02-0584250 INIST
ET :	The monoamine reuptake blocker brasofensine reverses akinesia without dyskinesia in MPTP-treated and levodopa-primed common marmosets
AU :	PEARCE (Ronald K. B.); SMITH (Lance A.); JACKSON (Michael J.); BANERJI (Tara); SCHEEL-KRÜGER (Jorgen); JENNER (Peter)
AF :	Division of Pharmacology and Therapeutics, Guy's, King's and St. Thomas' School of Biomedical Sciences/London/Royaume-Uni (1 aut., 2 aut., 3 aut., 4 aut., 6 aut.); Department of Neurology, Charing Cross Hospital/London/Royaume-Uni (1 aut.); NeuroSearch, Smedeland/Glostrup/Danemark (5 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2002; Vol. 17; No. 5; Pp. 877-886; Bibl. 55 ref.
LA :	Anglais
EA :	The common marmoset develops motor deficits after MPTP treatment and exhibits dyskinesia after chronic levodopa (L-dopa) dosing and subsequent re-challenge with L-dopa and other dopaminergic agents. We report on the actions of the potent monoamine reuptake blocker brasofensine on motor disability, locomotor activity, and dyskinesia in the 1-methyl-4-1, 2,3,6-tetrahydropyridine (MPTP) -treated marmoset model of Parkinson's disease. Oral administration of brasofensine (0.25, 0.5, 1.0, or 2.5 mg/kg) to MPTP-treated marmosets produced a long-lasting, dose-dependent increase in locomotor activity and reduction in disability scores. In addition, coadministration of the lowest dose of brasofensine (0.25 mg/kg orally) with a threshold oral dose of L-dopa (2.5 mg/kg) caused a marked increase in locomotor activity, greater than that produced by either drug alone. In other MPTP-treated marmosets previously primed to exhibit dyskinesia by repeated L-dopa dosing, brasofensine effectively reversed akinesia with a naturalistic and prolonged motor response without the appearance of dyskinesia or stereotypy. This finding contrasts with the severe dyskinesia, stereotypy, and hyperkinesis produced by equivalent doses of L-dopa. The ability of brasofensine to produce a prolonged and naturalistic antiparkinsonian response without eliciting dyskinesia after previous L-dopa priming may relate to actions on D₁ receptor-linked pathways. These findings suggest that monoamine reuptake blockade may be of value in the treatment of Parkinson's disease, both early in the disease course and when L-dopa-induced dyskinesias complicate treatment.
CC :	002B02B09A; 002B17G
FD :	Parkinson maladie; Dyskinésie; Brasofensine; Inhibiteur recapture; Dopamine; Antiparkinsonien; Pathologie expérimentale; Traitement; Animal; Singe; Chimiothérapie
FG :	Primates; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Trouble neurologique; Mouvement involontaire
ED :	Parkinson disease; Dyskinesia; Brasofensine; Reuptake inhibitor; Dopamine; Antiparkinson agent; Experimental disease; Treatment; Animal; Monkey; Chemotherapy
EG :	Primates; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Neurological disorder; Involuntary movement
SD :	Parkinson enfermedad; Disquinesia; Brasofensina; Inhibidor recaptura; Dopamina; Antiparkinsoniano; Patología experimental; Tratamiento; Animal; Mono; Quimioterapia
LO :	INIST-20953.354000105152380030
ID :	02-0584250

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Pascal:02-0584250

Le document en format XML

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<front><div type="abstract" xml:lang="en">The common marmoset develops motor deficits after MPTP treatment and exhibits dyskinesia after chronic levodopa (L-dopa) dosing and subsequent re-challenge with L-dopa and other dopaminergic agents. We report on the actions of the potent monoamine reuptake blocker brasofensine on motor disability, locomotor activity, and dyskinesia in the 1-methyl-4-1, 2,3,6-tetrahydropyridine (MPTP) -treated marmoset model of Parkinson's disease. Oral administration of brasofensine (0.25, 0.5, 1.0, or 2.5 mg/kg) to MPTP-treated marmosets produced a long-lasting, dose-dependent increase in locomotor activity and reduction in disability scores. In addition, coadministration of the lowest dose of brasofensine (0.25 mg/kg orally) with a threshold oral dose of L-dopa (2.5 mg/kg) caused a marked increase in locomotor activity, greater than that produced by either drug alone. In other MPTP-treated marmosets previously primed to exhibit dyskinesia by repeated L-dopa dosing, brasofensine effectively reversed akinesia with a naturalistic and prolonged motor response without the appearance of dyskinesia or stereotypy. This finding contrasts with the severe dyskinesia, stereotypy, and hyperkinesis produced by equivalent doses of L-dopa. The ability of brasofensine to produce a prolonged and naturalistic antiparkinsonian response without eliciting dyskinesia after previous L-dopa priming may relate to actions on D<sub>1</sub>
 receptor-linked pathways. These findings suggest that monoamine reuptake blockade may be of value in the treatment of Parkinson's disease, both early in the disease course and when L-dopa-induced dyskinesias complicate treatment.</div>
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 receptor-linked pathways. These findings suggest that monoamine reuptake blockade may be of value in the treatment of Parkinson's disease, both early in the disease course and when L-dopa-induced dyskinesias complicate treatment.</s0>
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<server><NO>PASCAL 02-0584250 INIST</NO>
<ET>The monoamine reuptake blocker brasofensine reverses akinesia without dyskinesia in MPTP-treated and levodopa-primed common marmosets</ET>
<AU>PEARCE (Ronald K. B.); SMITH (Lance A.); JACKSON (Michael J.); BANERJI (Tara); SCHEEL-KRÜGER (Jorgen); JENNER (Peter)</AU>
<AF>Division of Pharmacology and Therapeutics, Guy's, King's and St. Thomas' School of Biomedical Sciences/London/Royaume-Uni (1 aut., 2 aut., 3 aut., 4 aut., 6 aut.); Department of Neurology, Charing Cross Hospital/London/Royaume-Uni (1 aut.); NeuroSearch, Smedeland/Glostrup/Danemark (5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2002; Vol. 17; No. 5; Pp. 877-886; Bibl. 55 ref.</SO>
<LA>Anglais</LA>
<EA>The common marmoset develops motor deficits after MPTP treatment and exhibits dyskinesia after chronic levodopa (L-dopa) dosing and subsequent re-challenge with L-dopa and other dopaminergic agents. We report on the actions of the potent monoamine reuptake blocker brasofensine on motor disability, locomotor activity, and dyskinesia in the 1-methyl-4-1, 2,3,6-tetrahydropyridine (MPTP) -treated marmoset model of Parkinson's disease. Oral administration of brasofensine (0.25, 0.5, 1.0, or 2.5 mg/kg) to MPTP-treated marmosets produced a long-lasting, dose-dependent increase in locomotor activity and reduction in disability scores. In addition, coadministration of the lowest dose of brasofensine (0.25 mg/kg orally) with a threshold oral dose of L-dopa (2.5 mg/kg) caused a marked increase in locomotor activity, greater than that produced by either drug alone. In other MPTP-treated marmosets previously primed to exhibit dyskinesia by repeated L-dopa dosing, brasofensine effectively reversed akinesia with a naturalistic and prolonged motor response without the appearance of dyskinesia or stereotypy. This finding contrasts with the severe dyskinesia, stereotypy, and hyperkinesis produced by equivalent doses of L-dopa. The ability of brasofensine to produce a prolonged and naturalistic antiparkinsonian response without eliciting dyskinesia after previous L-dopa priming may relate to actions on D<sub>1</sub>
 receptor-linked pathways. These findings suggest that monoamine reuptake blockade may be of value in the treatment of Parkinson's disease, both early in the disease course and when L-dopa-induced dyskinesias complicate treatment.</EA>
<CC>002B02B09A; 002B17G</CC>
<FD>Parkinson maladie; Dyskinésie; Brasofensine; Inhibiteur recapture; Dopamine; Antiparkinsonien; Pathologie expérimentale; Traitement; Animal; Singe; Chimiothérapie</FD>
<FG>Primates; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Trouble neurologique; Mouvement involontaire</FG>
<ED>Parkinson disease; Dyskinesia; Brasofensine; Reuptake inhibitor; Dopamine; Antiparkinson agent; Experimental disease; Treatment; Animal; Monkey; Chemotherapy</ED>
<EG>Primates; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Neurological disorder; Involuntary movement</EG>
<SD>Parkinson enfermedad; Disquinesia; Brasofensina; Inhibidor recaptura; Dopamina; Antiparkinsoniano; Patología experimental; Tratamiento; Animal; Mono; Quimioterapia</SD>
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	Movement Disorders (revue)
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Movement Disorders (revue)

The monoamine reuptake blocker brasofensine reverses akinesia without dyskinesia in MPTP-treated and levodopa-primed common marmosets

The monoamine reuptake blocker brasofensine reverses akinesia without dyskinesia in MPTP-treated and levodopa-primed common marmosets

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