Martinez-Lopez Jesus E, Moreno-Bravo Juan A, Madrigal M Pilar, Martinez Salvador, Puelles Eduardo
Instituto de Neurociencias de Alicante, Universidad Miguel Hernandez, Consejo Superior de Investigaciones Científicas (UMH-CSIC) San Juan de Alicante, Alicante, Spain.
Instituto de Neurociencias de Alicante, Universidad Miguel Hernandez, Consejo Superior de Investigaciones Científicas (UMH-CSIC) San Juan de Alicante, Alicante, Spain ; Instituto Murciano de Investigación Biomédica Virgen de la Arrixaca IMIB-Arrixaca, Universidad de Murcia Murcia, Spain.
Front Neuroanat. 2015 Feb 5;9:8. doi: 10.3389/fnana.2015.00008. eCollection 2015.
The red nucleus (RN) is a neuronal population that plays an important role in forelimb motor control and locomotion. Histologically it is subdivided into two subpopulations, the parvocellular RN (pRN) located in the diencephalon and the magnocellular RN (mRN) in the mesencephalon. The RN integrates signals from motor cortex and cerebellum and projects to spinal cord interneurons and motor neurons through the rubrospinal tract (RST). Pou4f1 is a transcription factor highly expressed in this nucleus that has been related to its specification. Here we profoundly analyzed consequences of Pou4f1 loss-of-function in development, maturation and axonal projection of the RN. Surprisingly, RN neurons are specified and maintained in the mutant, no cell death was detected. Nevertheless, the nucleus appeared disorganized with a strong delay in radial migration and with a wider neuronal distribution; the neurons did not form a compacted population as they do in controls, Robo1 and Slit2 were miss-expressed. Cplx1 and Npas1, expressed in the RN, are transcription factors involved in neurotransmitter release, neuronal maturation and motor function processes among others. In our mutant mice, both transcription factors are lost, suggesting an abnormal maturation of the RN. The resulting altered nucleus occupied a wider territory. Finally, we examined RST development and found that the RN neurons were able to project to the spinal cord but their axons appeared defasciculated. These data suggest that Pou4f1 is necessary for the maturation of RN neurons but not for their specification and maintenance.
红核(RN)是一组在肢体运动控制和运动中起重要作用的神经元。从组织学上看,它可细分为两个亚群,位于间脑的小细胞红核(pRN)和中脑的大细胞红核(mRN)。红核整合来自运动皮层和小脑的信号,并通过红核脊髓束(RST)投射到脊髓中间神经元和运动神经元。Pou4f1是一种在该核中高度表达的转录因子,与该核的特化有关。在这里,我们深入分析了Pou4f1功能丧失对红核发育、成熟和轴突投射的影响。令人惊讶的是,红核神经元在突变体中得以特化并维持,未检测到细胞死亡。然而,该核出现结构紊乱,径向迁移严重延迟,神经元分布更广泛;神经元没有像在对照组中那样形成紧密的群体,Robo1和Slit2表达错误。在红核中表达的Cplx1和Npas1是参与神经递质释放、神经元成熟和运动功能等过程的转录因子。在我们的突变小鼠中,这两种转录因子都缺失了,这表明红核成熟异常。由此导致的核占据了更广泛的区域。最后,我们检查了红核脊髓束的发育,发现红核神经元能够投射到脊髓,但它们的轴突似乎出现了脱束现象。这些数据表明,Pou4f1对红核神经元的成熟是必需的,但对其特化和维持并非必需。