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Neural Plasticity
Volume 2018, Article ID 8561704, 8 pages
Research Article

Peripheral Nerve Injury-Induced Astrocyte Activation in Spinal Ventral Horn Contributes to Nerve Regeneration

1Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, Southern Medical University, Guangzhou 510515, China
2Department of Histology and Embryology, Southern Medical University, Guangzhou 510515, China
3Department of Histology and Embryology, Fujian University of Traditional Chinese Medicine, Fuzhou 350000, China
4Department of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong
5State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Pokfulam, Hong Kong
6Joint Laboratory of Jinan University and The University of Hong Kong, GHM Institute of CNS Regeneration, Jinan University, Guangzhou 510632, China
7Institute of Bone Biology, Academy of Orthopedics, Guangzhou, Guangdong Province 510665, China

Correspondence should be addressed to Jiasong Guo; moc.nuyila@ouggnosaij

Received 30 November 2017; Revised 3 February 2018; Accepted 20 February 2018; Published 3 April 2018

Academic Editor: Long-Jun Wu

Copyright © 2018 Changhui Qian et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Accumulating evidences suggest that peripheral nerve injury (PNI) may initiate astrocytic responses in the central nervous system (CNS). However, the response of astrocytes in the spinal ventral horn and its potential role in nerve regeneration after PNI remain unclear. Herein, we firstly illustrated that astrocytes in the spinal ventral horn were dramatically activated in the early stage following sciatic nerve injury, and these profiles were eliminated in the chronic stage. Additionally, we found that the expression of neurotrophins, including brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and neurotrophin-3 (NT-3), also accompanied with astrocyte activation. In comparison with the irreversible transected subjects, astrocyte activation and the neurotrophic upregulation in the early stage were more drastic in case the transected nerve was rebridged immediately after injury. Furthermore, administering fluorocitrate to inhibit astrocyte activation resulted in decreased neurotrophin expression in the spinal ventral horn and delayed axonal regeneration in the nerve as well as motor function recovery. Overall, the present study indicates that peripheral nerve injury can initiate astrocyte activation accompanied with neurotrophin upregulation in the spinal ventral horn. The above responses mainly occur in the early stage of PNI and may contribute to nerve regeneration and motor function recovery.