Modulation of CaMKIIa-GluN2B interaction in levodopa-induced dyskinesia in 6-OHDA-lesioned Parkinson's rats.
Biomed Pharmacother
; 107: 769-776, 2018 Nov.
Article
en En
| MEDLINE
| ID: mdl-30142538
ABSTRACT
Long-term treatment with L-dopa leads to involuntary aimless movements called L-dopa-induced dyskinesia (LID) has hindered its use in Parkinson's disease (PD) patients. Emerging evidence suggests a possible role of CaMKIIa and its interacting partners in the development of LID. In this study, we found that CaMKIIa was found to form complexes with GluN2B after chronic administration of L-dopa in adult rat striatal neurons. Intrastriatal injection of KN-93 significantly reduced the level of GluN2B in CaMKIIa precipitates with a dose dependent response, as well as reduced the Global ALO AIM score without ablation of the therapeutic response to L-dopa. In parallel, intrastriatal injection of MK-801 significantly alleviated the level of CaMKIIa in GluN2B precipitates compared to LID group (p < 0.01), and this is accompanied by realizing improvement of the Global ALO AIM score also without affect the efï¬cacy of L-dopa. In summary, the present study indicated that CaMKIIa-GluN2B interaction had an important role in the development of LID. Disrupt of this link by intrastriatal infusion of KN-93 or MK-801 ameliorated dyskinesia in 6-OHDA-lesioned PD rats.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Enfermedad de Parkinson
/
Receptores de N-Metil-D-Aspartato
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Discinesia Inducida por Medicamentos
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Proteína Quinasa Tipo 2 Dependiente de Calcio Calmodulina
Límite:
Animals
Idioma:
En
Revista:
Biomed Pharmacother
Año:
2018
Tipo del documento:
Article
País de afiliación:
China