Blockade of transient receptor potential cation channel subfamily V member 1 promotes regeneration after sciatic nerve injury

作     者：Fei Ren Hong Zhang Chao Qi Mei-ling Gao Hong Wang Xia-qing Li 

作者机构：Department of Pathophysiology School of Basic Medical Sciences Shanxi Medical University 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2015年第10卷第8期

页      面：1324-1331页

核心收录：

学科分类：1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

基　　金：supported by the National Natural Science Foundation of China,No.81171178 the Natural Science Foundation of Shanxi Province in China,No.2012011036-3 Scientific Research Foundation of Shanxi Province of China for the Returned Overseas Chinese Scholars,No.2013011054-2 

主　　题：nerve regeneration peripheral nerve regeneration transient receptor potential cation channel subfamily V member 1 capsaicin receptor vanilloid receptor TRPV1 antagonist nociceptor nerve crush injury Wallerian degeneration axon NSFC grant neurites neural regeneration 

摘      要：The transient receptor potential cation channel subfamily V member 1（TRPV1） provides the sensation of pain（nociception）. However, it remains unknown whether TRPV1 is activated after peripheral nerve injury, or whether activation of TRPV1 affects neural regeneration. In the present study, we established rat models of unilateral sciatic nerve crush injury, with or without pretreatment with AMG517（300 mg/kg）, a TRPV1 antagonist, injected subcutaneously into the ipsilateral paw 60 minutes before injury. At 1 and 2 weeks after injury, we performed immunofluorescence staining of the sciatic nerve at the center of injury, at 0.3 cm proximal and distal to the injury site, and in the dorsal root ganglia. Our results showed that Wallerian degeneration occurred distal to the injury site, and neurite outgrowth and Schwann cell regeneration occurred proximal to the injury. The number of regenerating myelinated and unmyelinated nerve clusters was greater in the AMG517-pretreated rats than in the vehicle-treated group, most notably 2 weeks after injury. TRPV1 expression in the injured sciatic nerve and ipsilateral dorsal root ganglia was markedly greater than on the contralateral side. Pretreatment with AMG517 blocked this effect. These data indicate that TRPV1 is activated or overexpressed after sciatic nerve crush injury, and that blockade of TRPV1 may accelerate regeneration of the injured sciatic nerve.