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<dc:title xml:lang="fr">Rôle du récepteur orphelin GPR88 dans les pathologies psychiatriques et motrices</dc:title>
<dcterms:alternative xml:lang="en">Role of the orphan receptor GPR88 in psychiatric and motor disorders</dcterms:alternative>
<dc:subject xml:lang="fr">Récepteur couplé à protéine G</dc:subject>
<dc:subject xml:lang="fr">Anxiété</dc:subject>
<dc:subject xml:lang="fr">Coordination motrice</dc:subject>
<dc:subject xml:lang="fr">Inhibition du prépulse</dc:subject>
<dc:subject xml:lang="fr">Striatum</dc:subject>
<dc:subject xml:lang="fr">Neurones moyen épineux</dc:subject>
<dc:subject xml:lang="en">G protein coupled receptor</dc:subject>
<dc:subject xml:lang="en">Anxiety</dc:subject>
<dc:subject xml:lang="en">Motor coordination</dc:subject>
<dc:subject xml:lang="en">Prepulse inhibition</dc:subject>
<dc:subject xml:lang="en">Striatum</dc:subject>
<dc:subject xml:lang="en">Medium spiny neurons</dc:subject>
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<dcterms:abstract xml:lang="fr">GPR88 est un récepteur couplé aux protéines G orphelin exprimé principalement au niveau du striatum spécifiquement dans les neurones moyens épineux de la voie striato-nigrale et de la voie striato-pallidale.Premièrement nous avons étudié les souris Gpr88 KO et montré des altérations biochimiques, structurales et comportementales. Aussi les résultats montrent que l’hyperactivité des souris Gpr88 KO est diminuée par l’administration de méthylphénidate. Deuxièmement nous avons montré que la diminution des comportements liés à l’anxiété dépend de GPR88 dans la voie striato-pallidale et que la coordination motrice est régulée par GPR88 dans le striatum adulte (injection AAV-Cre) et dans la voie striato-pallidale. Dernièrement, nous avons confirmé un déficit d’inhibition du prépulse chez les souris Gpr88 KO, mais aussi montré que celui-ci s’étend à la modalité visuelle et n’est pas lié à un déficit général d’inhibition ou à la délétion de Gpr88 dans les neurones striato-pallidaux.</dcterms:abstract>
<dcterms:abstract xml:lang="en">Among brain orphan G protein-coupled receptors, GPR88 shows high expression mainly in the striatum specifically in medium spiny neurons of both the striatonigral and striatopallidal pathwaysFirst, we examine full Gpr88 KO mice and show biochemical, structural and behavioral alterations. Results also show that the hyperactivity phenotype of Gpr88 KO mice is reversed by methylphenidate.Second, we show that Gpr88 in striatopallidal neurons (cKO approach) exerts anxiogénic activity and that motor coordination is regulated by GPR88 in the adult brain (AAV-Cre approach) and in the striatopallidal pathway.Finally, we confirmed previous data showing impaired acoustic prepulse inhibition in Gpr88 KO mice and further show that this deficit is not the result of a general inhibition deficit or of the lack of GPR88 in striatopallidal neurons.</dcterms:abstract>
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