Mahmoudi Souha, Samadi Pershia, Gilbert François, Ouattara Bazoumana, Morissette Marc, Grégoire Laurent, Rouillard Claude, Di Paolo Thérèse, Lévesque Daniel
Faculty of Pharmacy, Université de Montréal, Montreal, Quebec, Canada.
Neurobiol Dis. 2009 Oct;36(1):213-22. doi: 10.1016/j.nbd.2009.07.017. Epub 2009 Jul 25.
We have previously shown that docosahexaenoic acid (DHA) significantly reduced L-Dopa-induced dyskinesia (LID) in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkeys (Samadi et al., Ann. Neurol. 59:282-288, 2006). In the present study, we measured for the first time mRNA levels of Nur77, an orphan nuclear receptor that participates to adaptive and/or aberrant dopamine-related behaviors, and retinoid X receptor gamma1 (RXRgamma1), a putative brain receptor for DHA and transcriptional partner of Nur77, in MPTP monkeys treated with L-Dopa and DHA. The RXRgamma1 mRNA is strongly expressed in monkey caudate nucleus and putamen, but no change in levels of RXRgamma1 was observed following MPTP and L-Dopa treatments. On the other hand, denervation reduced Nur77 mRNA levels, whereas chronic L-Dopa treatment strongly induced Nur77 transcripts. These modulations are taking place in substance P positive cells and are associated with both caudate-putamen matrix and striosome compartments. Interestingly, combination of L-Dopa with DHA further increases Nur77 mRNA levels in the anterior caudate-putamen, and mainly in striosomes. This is accompanied by a significant inverse correlation between Nur77 mRNA levels and dyskinetic scores. Taken together, our results show that Nur77 expression is modulated following dopamine denervation and chronic L-Dopa therapy in a non-human primate model of Parkinson's disease, and suggest that strong modulation of Nur77 expression might be linked to a reduced risk to develop LIDs.
我们之前已经表明,二十二碳六烯酸(DHA)可显著降低1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)处理的猴子中左旋多巴诱导的异动症(LID)(Samadi等人,《神经病学纪事》59:282 - 288,2006年)。在本研究中,我们首次测量了用左旋多巴和DHA处理的MPTP猴子中Nur77(一种参与适应性和/或异常多巴胺相关行为的孤儿核受体)以及视黄酸X受体γ1(RXRγ1,一种推测的DHA脑受体和Nur77的转录伴侣)的mRNA水平。RXRγ1 mRNA在猴子尾状核和壳核中强烈表达,但在MPTP和左旋多巴处理后未观察到RXRγ1水平的变化。另一方面,去神经支配降低了Nur77 mRNA水平,而慢性左旋多巴处理强烈诱导了Nur77转录本。这些调节发生在P物质阳性细胞中,并且与尾状核 - 壳核基质和纹状体小体区室都有关。有趣的是,左旋多巴与DHA联合使用进一步增加了前尾状核 - 壳核中,主要是纹状体小体中的Nur77 mRNA水平。这伴随着Nur77 mRNA水平与异动症评分之间显著的负相关。综上所述,我们的结果表明,在帕金森病的非人灵长类动物模型中,多巴胺去神经支配和慢性左旋多巴治疗后Nur77表达受到调节,并提示Nur强烈调节77表达可能与降低发生LID的风险有关。