ParkinsonFranceV1, Main, Exploration, bibRecord, 000709

Are cyclooxygenase-2 and nitric oxide involved in the dyskinesia of Parkinson's disease induced by l-DOPA?†

Identifieur interne : 000709 ( Main/Exploration ); précédent : 000708; suivant : 000710

Are cyclooxygenase-2 and nitric oxide involved in the dyskinesia of Parkinson's disease induced by l-DOPA?†

Auteurs : Mariza Bortolanza [Brésil] ; Fernando E. Padovan-Neto [Brésil] ; Roberta Cavalcanti-Kiwiatkoski [Brésil] ; Maurício Dos Santos-Pereira [Brésil] ; Miso Mitkovski [Allemagne] ; Rita Raisman-Vozari [France] ; Elaine Del-Bel [Brésil]

Source :

Philosophical Transactions of the Royal Society B: Biological Sciences [ 0962-8436 ] ; 2015.

RBID : PMC:4455759

Abstract

Inflammatory mechanisms are proposed to play a role in l-DOPA-induced dyskinesia. Cyclooxygenase-2 (COX2) contributes to inflammation pathways in the periphery and is constitutively expressed in the central nervous system. Considering that inhibition of nitric oxide (NO) formation attenuates l-DOPA-induced dyskinesia, this study aimed at investigating if a NO synthase (NOS) inhibitor would change COX2 brain expression in animals with l-DOPA-induced dyskinesia. To this aim, male Wistar rats received unilateral 6-hydroxydopamine microinjection into the medial forebrain bundle were treated daily with l-DOPA (21 days) combined with 7-nitroindazole or vehicle. All hemi-Parkinsonian rats receiving l-DOPA showed dyskinesia. They also presented increased neuronal COX2 immunoreactivity in the dopamine-depleted dorsal striatum that was directly correlated with dyskinesia severity. Striatal COX2 co-localized with choline-acetyltransferase, calbindin and DARPP-32 (dopamine-cAMP-regulated phosphoprotein-32), neuronal markers of GABAergic neurons. NOS inhibition prevented l-DOPA-induced dyskinesia and COX2 increased expression in the dorsal striatum. These results suggest that increased COX2 expression after l-DOPA long-term treatment in Parkinsonian-like rats could contribute to the development of dyskinesia.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4455759

DOI: 10.1098/rstb.2014.0190
PubMed: 26009769
PubMed Central: 4455759

Affiliations:

Allemagne, Brésil, France

Le document en format XML

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<front><div type="abstract" xml:lang="en"><p>Inflammatory mechanisms are proposed to play a role in <sc>l</sc>
-DOPA-induced dyskinesia. Cyclooxygenase-2 (COX2) contributes to inflammation pathways in the periphery and is constitutively expressed in the central nervous system. Considering that inhibition of nitric oxide (NO) formation attenuates <sc>l</sc>
-DOPA-induced dyskinesia, this study aimed at investigating if a NO synthase (NOS) inhibitor would change COX2 brain expression in animals with <sc>l</sc>
-DOPA-induced dyskinesia. To this aim, male Wistar rats received unilateral 6-hydroxydopamine microinjection into the medial forebrain bundle were treated daily with <sc>l</sc>
-DOPA (21 days) combined with 7-nitroindazole or vehicle. All hemi-Parkinsonian rats receiving <sc>l</sc>
-DOPA showed dyskinesia. They also presented increased neuronal COX2 immunoreactivity in the dopamine-depleted dorsal striatum that was directly correlated with dyskinesia severity. Striatal COX2 co-localized with choline-acetyltransferase, calbindin and DARPP-32 (dopamine-cAMP-regulated phosphoprotein-32), neuronal markers of GABAergic neurons. NOS inhibition prevented <sc>l</sc>
-DOPA-induced dyskinesia and COX2 increased expression in the dorsal striatum. These results suggest that increased COX2 expression after <sc>l</sc>
-DOPA long-term treatment in Parkinsonian-like rats could contribute to the development of dyskinesia.</p>
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La maladie de Parkinson en France (serveur d'exploration)

Are cyclooxygenase-2 and nitric oxide involved in the dyskinesia of Parkinson's disease induced by l-DOPA?†

Are cyclooxygenase-2 and nitric oxide involved in the dyskinesia of Parkinson's disease induced by l-DOPA?†

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	La maladie de Parkinson en France (serveur d'exploration)
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