Striatal Neurons Expressing D(1) and D(2) Receptors are Morphologically Distinct and Differently Affected by Dopamine Denervation in Mice.
Striatal Neurons Expressing D(1) and D(2) Receptors are Morphologically Distinct and Differently Affected by Dopamine Denervation in Mice.
复制标题
表达D（1）和D（2）受体的纹状体神经元在形态上是不同的，并且受小鼠多巴胺神经化的影响不同。
DOI：
10.1038/srep41432
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发表时间：
2017-01-27
影响因子：
4.6
通讯作者：
Parent M
中科院分区：
文献类型：
--
作者：
Gagnon D;Petryszyn S;Sanchez MG;Bories C;Beaulieu JM;De Koninck Y;Parent A;Parent M
帕金森氏病中黑质纹状体多巴胺神经元的丧失导致表达D1或D2多巴胺受体的纹状体中棘神经元（MSN）上树突棘数量减少。目前尚不清楚表达两种受体（D1/D2 MSN）的MSN的后果。我们通过比较6-OHDA损伤的双BAC转基因小鼠（Drd 1a-tdTomato/Drd 2-EGFP）与假损伤动物，寻找多巴胺去神经诱导的D1/D2 MSNs密度、区域分布和形态学特征的变化。D1/D2 MSN均匀分布在整个背侧纹状体（MSN的1.9%）。相反，它们分布不均匀，在腹侧纹状体中数量更多（壳中占14.6%，核心中占7.3%）。与D1和D2 MSN相比，D1/D2 MSN具有较小的细胞体和较少的树枝状树突树，树突棘较少。在6-OHDA损伤的小鼠中，D1/D2 MSNs以及D1和D2 MSNs的树突棘密度显著降低。与D1和D2 MSN相反，D1/D2 MSN的树突状分支的程度在6-OHDA损伤的小鼠中似乎没有改变。我们的数据表明，D1/D2 MSNs在小鼠纹状体形成一个独特的神经元群体，受到不同的多巴胺传入阻滞，帕金森氏病的特点。
The loss of nigrostriatal dopamine neurons in Parkinson’s disease induces a reduction in the number of dendritic spines on medium spiny neurons (MSNs) of the striatum expressing D1 or D2 dopamine receptor. Consequences on MSNs expressing both receptors (D1/D2 MSNs) are currently unknown. We looked for changes induced by dopamine denervation in the density, regional distribution and morphological features of D1/D2 MSNs, by comparing 6-OHDA-lesioned double BAC transgenic mice (Drd1a-tdTomato/Drd2-EGFP) to sham-lesioned animals. D1/D2 MSNs are uniformly distributed throughout the dorsal striatum (1.9% of MSNs). In contrast, they are heterogeneously distributed and more numerous in the ventral striatum (14.6% in the shell and 7.3% in the core). Compared to D1 and D2 MSNs, D1/D2 MSNs are endowed with a smaller cell body and a less profusely arborized dendritic tree with less dendritic spines. The dendritic spine density of D1/D2 MSNs, but also of D1 and D2 MSNs, is significantly reduced in 6-OHDA-lesioned mice. In contrast to D1 and D2 MSNs, the extent of dendritic arborization of D1/D2 MSNs appears unaltered in 6-OHDA-lesioned mice. Our data indicate that D1/D2 MSNs in the mouse striatum form a distinct neuronal population that is affected differently by dopamine deafferentation that characterizes Parkinson’s disease.