Axonal Growth and Regeneration, German Center for Neurodegenerative Diseases, 53175 Bonn, Germany.
Genomics and Immunoregulation, LIMES-Institute, University of Bonn, 53115 Bonn, Germany.
Neuron. 2016 Oct 19;92(2):419-434. doi: 10.1016/j.neuron.2016.09.026. Epub 2016 Oct 6.
Injuries to the adult CNS often result in permanent disabilities because neurons lose the ability to regenerate their axon during development. Here, whole transcriptome sequencing and bioinformatics analysis followed by gain- and loss-of-function experiments identified Cacna2d2, the gene encoding the Alpha2delta2 subunit of voltage-gated calcium channels (VGCCs), as a developmental switch that limits axon growth and regeneration. Cacna2d2 gene deletion or silencing promoted axon growth in vitro. In vivo, Alpha2delta2 pharmacological blockade through Pregabalin (PGB) administration enhanced axon regeneration in adult mice after spinal cord injury (SCI). As PGB is already an established treatment for a wide range of neurological disorders, our findings suggest that targeting Alpha2delta2 may be a novel treatment strategy to promote structural plasticity and regeneration following CNS trauma.
成人中枢神经系统损伤常导致永久性残疾,因为神经元在发育过程中丧失了再生轴突的能力。在这里,通过全转录组测序和生物信息学分析,以及功能获得和缺失实验,确定 Cacna2d2 基因(编码电压门控钙通道 (VGCC) 的 Alpha2delta2 亚基)是一个发育开关,限制轴突生长和再生。Cacna2d2 基因缺失或沉默促进了体外轴突生长。在体内,通过给予普瑞巴林(Pregabalin,PGB)阻断 Alpha2delta2 可增强成年小鼠脊髓损伤后的轴突再生。由于 PGB 已经是治疗多种神经疾病的成熟药物,我们的发现表明,靶向 Alpha2delta2 可能是一种促进中枢神经系统创伤后结构可塑性和再生的新治疗策略。