Genetic deletion of Rhes or pharmacological blockade of mTORC1 prevent striato-nigral neurons activation in levodopa-induced dyskinesia
详细信息 查看全文
- 作者：Alberto Brugnolia ; Francesco Napolitanob ; c ; Alessandro Usiellob ; d ; Michele Moraria ; m.morari@unife.it" class="auth_mail" title="E-mail the corresponding author
- 关键词：AIMs ; abnormal involuntary movements ; DA ; dopamine ; DARPP-32 ; dopamine and cAMP-regulated phosphoprotein ; Mr 32 ; kDa ; D1R ; D1 receptor ; D2R ; D2 receptor ; ERK ; extracellular-regulated kinase ; L-DOPA ; levodopa ; LID ; levodopa-induced dyskinesia ; MSNs ; medium-sized spiny neurons ; mTORC1 ; mammalian target of rapamycin complex 1 ; 6-OHDA ; 6-hydroxydopamine ; PD ; Parkinson's disease ; Rhes ; Ras homolog enriched in striatum ; SNr ; substantia nigra pars reticulata
- 刊名：Neurobiology of Disease
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：85
- 期：Complete
- 页码：155-163
- 全文大小：1030 K
文摘
- •
Rhes deletion and mTORC1 blockade attenuate levodopa-induced dyskinesia in mice.
- •
Rapamycin but not Rhes deletion fully preserves rotarod performance on levodopa.
- •
Rhes deletion and rapamycin prevent the levodopa-induced rise of nigral amino acids.
- •
Rapamycin but not Rhes deletion prevents the rise of striatal glutamate.