NeuroD1 overexpression in spinal neurons accelerates axonal r

AAV-Cre was used to speciﬁcally transfect neurons in the lumbar spinal cord. (From BrainVTA)

The viruses used from BrainVTA in this article are in the table below

CRE Recombinase

PT-0136 rAAV-SYN-Cre-WPE-pA

Muhua Lai, Mengjie Pan, Longjiao Ge, Jingmin Liu, Junyao Deng, Xianghai Wang, Lixia Li, Jinkun Wen, Dandan Tan, Haowen Zhang, Xiaofang Hu, Lanya Fu, Yizhou Xu, Zhenlin Li, Xiaozhong Qiu, Gong Chen, Jiasong Guo
Pub Date: 2020-01-25, DOI: 10.1016/j.expneurol.2020.113215, Email: [email protected]

Neurogenic differentiation 1 (NeuroD1) is mainlyexpressed in developing neurons where it plays critical roles in neuronal maturation and neurite elongation. The potential role and mechanism of NeuroD1 in adult axonal regeneration is not clear. The present study used synapsin (SYN) Cre and AAV9-Flex vectors to conditionally overexpress NeuroD1 in adult spinal neurons and found that NeuroD1 overexpression significantly accelerated axonal regeneration and functional recovery after sciatic nerve injury. Further in vitro and in vivo experiments suggested that the mechanism of NeuroD1 promotion on axonal regeneration was related to its regulation of the expression of neurotrophin BDNF and its receptor TrkB as well as a microtubule severing protein spastin.

Figure 1. A representative image shows that the sensory neurons in dorsal root ganglian (DRG) were not labeled with mCherry after the AAV9 vector was microinjected into the spinal cord.

This study is aimed to explore the potential role and mechanism of NeuroD1 in adult axonal regeneration. The present study demonstrated that AAV9 vector-mediated NeuroD1 overexpression in adult spinal neurons signiﬁcantly accelerated axonal regeneration and functional recovery after peripheral nerve injury. The present data also illustrated that NeuroD1 overexpression in spinal neurons resulted in the upregulation of BDNF, TrkB and spastin, which indicated that NeuroD1 accelerated axonal regeneration via regulating the expression of a neurotrophin and a microtubule severing protein.

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