Antidyskinetic effect of A2A and 5HT1A/1B receptor ligands in two animal models of Parkinson's disease.
Identifieur interne : 000093 ( Hal/Corpus ); précédent : 000092; suivant : 000094Antidyskinetic effect of A2A and 5HT1A/1B receptor ligands in two animal models of Parkinson's disease.
Auteurs : Annalisa Pinna ; Wai Kin D. Ko ; Giulia Costa ; Elisabetta Tronci ; Camino Fidalgo ; Nicola Simola ; Qin Li ; Mojgan Aghazadeh Tabrizi ; Erwan Bezard ; Manolo Carta ; Micaela MorelliSource :
- Movement Disorders [ 0885-3185 ] ; 2016-02-12.
Abstract
The serotonin 5-HT1A/1B receptor agonist eltoprazine suppressed dyskinetic-like behavior in animal models of Parkinson's disease (PD) but simultaneously reduced levodopa (l-dopa)-induced motility. Moreover, adenosine A2A receptor antagonists, such as preladenant, significantly increased l-dopa efficacy in PD without exacerbating dyskinetic-like behavior. We evaluated whether a combination of eltoprazine and preladenant may prevent or suppress l-dopa-induced dyskinesia, without impairing l-dopa's efficacy in relieving motor signs, in 2 PD models: unilateral 6-hydroxydopamine-lesioned rats and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys. Rotational behavior and abnormal involuntary movements, or disability and l-dopa-induced dyskinesia were evaluated in 6-hydroxydopamine-lesioned rats and MPTP-treated monkeys, respectively. Moreover, in the rodent striatum, induction of immediate-early gene zif-268, an index of long-term changes, was correlated with dyskinesia. In 6-hydroxydopamine-lesioned rats, combined administration of l-dopa (4 mg/kg) plus eltoprazine (0.6 mg/kg) plus preladenant (0.3 mg/kg) significantly prevented or reduced dyskinetic-like behavior without impairing motor activity. Zif-268 was increased in the striatum of rats treated with l-dopa and l-dopa plus preladenant compared with vehicle. In contrast, rats treated with eltoprazine (with or without preladenant) had lower zif-268 activation after chronic treatment in both the dyskinetic and l-dopa-non-primed groups. Moreover, acute l-dopa plus eltoprazine plus preladenant prevented worsening of motor performance (adjusting step) and sensorimotor integration deficit. Similar results were obtained in MPTP-treated monkeys, where a combination of preladenant with eltoprazine was found to counteract dyskinesia and maintain the full therapeutic effects of a low dose of l-dopa. Our results suggest a promising nondopaminergic pharmacological strategy for the treatment of dyskinesia in PD. © 2016 International Parkinson and Movement Disorder Society.
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DOI: 10.1002/mds.26475
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<front><div type="abstract" xml:lang="en">The serotonin 5-HT1A/1B receptor agonist eltoprazine suppressed dyskinetic-like behavior in animal models of Parkinson's disease (PD) but simultaneously reduced levodopa (l-dopa)-induced motility. Moreover, adenosine A2A receptor antagonists, such as preladenant, significantly increased l-dopa efficacy in PD without exacerbating dyskinetic-like behavior. We evaluated whether a combination of eltoprazine and preladenant may prevent or suppress l-dopa-induced dyskinesia, without impairing l-dopa's efficacy in relieving motor signs, in 2 PD models: unilateral 6-hydroxydopamine-lesioned rats and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys. Rotational behavior and abnormal involuntary movements, or disability and l-dopa-induced dyskinesia were evaluated in 6-hydroxydopamine-lesioned rats and MPTP-treated monkeys, respectively. Moreover, in the rodent striatum, induction of immediate-early gene zif-268, an index of long-term changes, was correlated with dyskinesia. In 6-hydroxydopamine-lesioned rats, combined administration of l-dopa (4 mg/kg) plus eltoprazine (0.6 mg/kg) plus preladenant (0.3 mg/kg) significantly prevented or reduced dyskinetic-like behavior without impairing motor activity. Zif-268 was increased in the striatum of rats treated with l-dopa and l-dopa plus preladenant compared with vehicle. In contrast, rats treated with eltoprazine (with or without preladenant) had lower zif-268 activation after chronic treatment in both the dyskinetic and l-dopa-non-primed groups. Moreover, acute l-dopa plus eltoprazine plus preladenant prevented worsening of motor performance (adjusting step) and sensorimotor integration deficit. Similar results were obtained in MPTP-treated monkeys, where a combination of preladenant with eltoprazine was found to counteract dyskinesia and maintain the full therapeutic effects of a low dose of l-dopa. Our results suggest a promising nondopaminergic pharmacological strategy for the treatment of dyskinesia in PD. © 2016 International Parkinson and Movement Disorder Society. </div>
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<sourceDesc> <biblStruct> <analytic> <title xml:lang="en">Antidyskinetic effect of A2A and 5HT1A/1B receptor ligands in two animal models of Parkinson's disease.</title>
<author role="aut"> <persName> <forename type="first">Annalisa</forename>
<surname>Pinna</surname>
</persName>
<idno type="halauthorid">1309319</idno>
<affiliation ref="#struct-344278"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Wai Kin D</forename>
<surname>Ko</surname>
</persName>
<idno type="halauthorid">1307955</idno>
<affiliation ref="#struct-439125"></affiliation>
<affiliation ref="#struct-439190"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Giulia</forename>
<surname>Costa</surname>
</persName>
<idno type="halauthorid">1309320</idno>
<affiliation ref="#struct-452953"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Elisabetta</forename>
<surname>Tronci</surname>
</persName>
<idno type="halauthorid">1059977</idno>
<affiliation ref="#struct-452954"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Camino</forename>
<surname>Fidalgo</surname>
</persName>
<idno type="halauthorid">1309321</idno>
<affiliation ref="#struct-452954"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Nicola</forename>
<surname>Simola</surname>
</persName>
<idno type="halauthorid">1232297</idno>
</author>
<author role="aut"> <persName> <forename type="first">Qin</forename>
<surname>Li</surname>
</persName>
<idno type="halauthorid">224848</idno>
<affiliation ref="#struct-439125"></affiliation>
<affiliation ref="#struct-439190"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Mojgan Aghazadeh</forename>
<surname>Tabrizi</surname>
</persName>
<idno type="halauthorid">1309322</idno>
<affiliation ref="#struct-452955"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Erwan</forename>
<surname>Bezard</surname>
</persName>
<idno type="halauthorid">537314</idno>
<affiliation ref="#struct-244085"></affiliation>
<affiliation ref="#struct-439125"></affiliation>
<affiliation ref="#struct-439190"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Manolo</forename>
<surname>Carta</surname>
</persName>
<idno type="halauthorid">1190816</idno>
<affiliation ref="#struct-452954"></affiliation>
</author>
<author role="aut"> <persName> <forename type="first">Micaela</forename>
<surname>Morelli</surname>
</persName>
<idno type="halauthorid">1309323</idno>
<affiliation ref="#struct-344278"></affiliation>
<affiliation ref="#struct-452953"></affiliation>
</author>
</analytic>
<monogr> <idno type="halJournalId" status="VALID">17211</idno>
<idno type="issn">0885-3185</idno>
<idno type="eissn">1531-8257</idno>
<title level="j">Movement Disorders</title>
<imprint> <publisher>Wiley</publisher>
<date type="datePub">2016-02-12</date>
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<idno type="pubmed">26871939</idno>
<idno type="doi">10.1002/mds.26475</idno>
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<abstract xml:lang="en">The serotonin 5-HT1A/1B receptor agonist eltoprazine suppressed dyskinetic-like behavior in animal models of Parkinson's disease (PD) but simultaneously reduced levodopa (l-dopa)-induced motility. Moreover, adenosine A2A receptor antagonists, such as preladenant, significantly increased l-dopa efficacy in PD without exacerbating dyskinetic-like behavior. We evaluated whether a combination of eltoprazine and preladenant may prevent or suppress l-dopa-induced dyskinesia, without impairing l-dopa's efficacy in relieving motor signs, in 2 PD models: unilateral 6-hydroxydopamine-lesioned rats and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys. Rotational behavior and abnormal involuntary movements, or disability and l-dopa-induced dyskinesia were evaluated in 6-hydroxydopamine-lesioned rats and MPTP-treated monkeys, respectively. Moreover, in the rodent striatum, induction of immediate-early gene zif-268, an index of long-term changes, was correlated with dyskinesia. In 6-hydroxydopamine-lesioned rats, combined administration of l-dopa (4 mg/kg) plus eltoprazine (0.6 mg/kg) plus preladenant (0.3 mg/kg) significantly prevented or reduced dyskinetic-like behavior without impairing motor activity. Zif-268 was increased in the striatum of rats treated with l-dopa and l-dopa plus preladenant compared with vehicle. In contrast, rats treated with eltoprazine (with or without preladenant) had lower zif-268 activation after chronic treatment in both the dyskinetic and l-dopa-non-primed groups. Moreover, acute l-dopa plus eltoprazine plus preladenant prevented worsening of motor performance (adjusting step) and sensorimotor integration deficit. Similar results were obtained in MPTP-treated monkeys, where a combination of preladenant with eltoprazine was found to counteract dyskinesia and maintain the full therapeutic effects of a low dose of l-dopa. Our results suggest a promising nondopaminergic pharmacological strategy for the treatment of dyskinesia in PD. © 2016 International Parkinson and Movement Disorder Society. </abstract>
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