Exercise attenuates levodopa-induced dyskinesia in 6-hydroxydopamine-lesioned mice

l-DOPA alleviates the motor symptoms of Parkinson’s disease, but its long-term use is associated with undesirable dyskinesia. We now tested whether exercise can attenuate this l-DOPA-induced dyskinesia (LID). We tested the effects of exercise on LID in 6-hydroxydopamine hydrochloride-hemiparkinsonia...

ver descrição completa

Detalhes bibliográficos
Autor principal: Jr., A. S. Aguiar (author)
Outros Autores: Moreira, E. L. G. (author), Hoeller, A. A. (author), Oliveira, P. A. (author), Córdova, F. M. (author), Glaser, V. (author), Walz, R. (author), Cunha, R. A. (author), Leal, R. B. (author), Latini, A. (author), Prediger, R. D. S. (author)
Formato: article
Idioma:por
Publicado em: 2013
Assuntos:
DARPP-32
dyskinesia
exercise
l-DOPA
Parkinson’s disease
6-OHDA
Texto completo:http://hdl.handle.net/10316/27237
País:Portugal
Oai:oai:estudogeral.sib.uc.pt:10316/27237
Descrição
Resumo:l-DOPA alleviates the motor symptoms of Parkinson’s disease, but its long-term use is associated with undesirable dyskinesia. We now tested whether exercise can attenuate this l-DOPA-induced dyskinesia (LID). We tested the effects of exercise on LID in 6-hydroxydopamine hydrochloride-hemiparkinsonian mice. Animals were treated with l-DOPA/benserazide (25/12.5 mg/kg, i.p.) without and with possibility to exercise (running wheel) during 2 weeks. Exercise drastically prevented the development of LID, and its associated aberrant striatal signaling, namely the hyperphosphorylation of dopamine and cAMP-regulated phosphoprotein 32 kDa protein and c-Fos expression. Our results indicate that exercise can partially prevent the development of LID through the normalization of striatopallidal dopaminergic signaling.

Registros relacionados