Palmitoyl serotonin inhibits L-dopa-induced abnormal involuntary movements in the mouse Parkinson model

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dc.contributor.authorHye-Yeon Park-
dc.contributor.authorYoung-Kyoung Ryu-
dc.contributor.authorJun Go-
dc.contributor.authorE Son-
dc.contributor.authorKyoung Shim Kim-
dc.contributor.authorM R Kim-
dc.description.abstractL-3,4-dihydroxyphenylalanine (L-DOPA) is the most common treatment for patients with Parkinson's disease (PD). However, long term use of L-DOPA for PD therapy lead to abnormal involuntary movements (AIMs) known as dyskinesia. Fatty acid amide hydrolase (FAAH) is enriched protein in basal ganglia, and inhibition of the protein reduces dyskinetic behavior of mice. Palmitoyl serotonin (PA-5HT) is a hybrid molecule patterned after arachidonoyl serotonin, antagonist of FAAH. However, the effect of PA- 5HT on L-DOPA-induced dyskinesia (LID) in PD have not yet been elucidated. To investigate whether PA-5HT relieve LID in PD and decrease hyperactivation of dopamine D1 receptors, we used the 6-hydroxydopomine (6-OHDA)-lesioned mouse model of PD and treated the L-DOPA (20 mg/kg) for 10 days with PA-5HT (0.3 mg/kg/day). The number of wall contacts with the forelimb in the cylinder test was significantly decreased by 6-OHDA lesion in mice and the pharmacotherapeutic effect of L-DOPA was also revealed in PA-5HT-treated mice. Moreover, in AIMs test, PA-5HT-treated mice showed significant reduction of locomotive, axial, limb, and orofacial AIMs score compared to the vehicle-treated mice. LID-induced hyper-phosphorylation of ERK1/2 and overexpression of FosB/ΔFosB was markedly decreased in 6-OHDA-lesioned striatum of PA-5HT-treated mice, indicating that PA- 5HT decreased the dopamine D1 receptor-hyperactivation induced by chronic treatment of L-DOPA in dopamine-denervated striatum. These results suggest that PA-5HT effectively attenuates the development of LID and enhance of ERK1/2 phosphorylation and FosB/ΔFosB expression in the hemi-parkinsonian mouse model. PA-5HT may have beneficial effect on the LID in PD.-
dc.publisherKorea Soc-Assoc-Inst-
dc.titlePalmitoyl serotonin inhibits L-dopa-induced abnormal involuntary movements in the mouse Parkinson model-
dc.title.alternativePalmitoyl serotonin inhibits L-dopa-induced abnormal involuntary movements in the mouse Parkinson model-
dc.citation.titleExperimental Neurobiology-
dc.contributor.affiliatedAuthorHye-Yeon Park-
dc.contributor.affiliatedAuthorYoung-Kyoung Ryu-
dc.contributor.affiliatedAuthorJun Go-
dc.contributor.affiliatedAuthorKyoung Shim Kim-
dc.identifier.bibliographicCitationExperimental Neurobiology, vol. 25, no. 4, pp. 174-184-
dc.subject.keywordpalmitoyl serotonin-
dc.subject.keywordL-DOPA-induced dyskinesia-
dc.subject.keywordParkinson’s disease-
dc.subject.localpalmitoyl serotonin-
dc.subject.locall-DOPA-induced dyskinesia-
dc.subject.localL-DOPA-induced dyskinesia-
dc.subject.localParkinson's disease-
dc.subject.localParkinsons disease (PD)-
dc.subject.localParkinsons disease-
dc.subject.localParkinson disease-
dc.subject.localParkinson’s diseases-
dc.subject.localParkinson’s Disease-
dc.subject.localParkinson's diasease-
dc.subject.localParkinson’s disease-
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Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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