降钙素基因相关肽
脊髓
神经科学
脊髓损伤
背根神经节
神经保护
医学
细胞生物学
生物
内科学
神经肽
受体
作者
Haoyu Xu,Yang Yang,Qingwen Deng,Baobao Zhang,Jingwen Ruan,Hui Jin,Junhua Wang,Jiale Ren,Bin Jiang,Jia-Hui Sun,Yuan‐Shan Zeng,Ying Ding
标识
DOI:10.1089/neu.2020.7155
摘要
results showed that CGRP would act on the post-synaptic spinal cord neurons and triggered the synthesis and secretion of neurotrophin-3 (NT-3) by activating the calcitonin gene-related peptide (CGRP)/ receptor activity-modifying protein (RAMP)1/calcium/calmodulin-dependent protein kinase (αCaMKII) pathway. Remarkably, the observed effect was prevented by the dorsal rhizotomy and the blockers of the CGRP/RAMP1/αCaMKII pathway. More importantly, increase in NT-3 promoted the survival, axonal regrowth, and synaptic maintenance of spinal cord neurons in the injured spinal cord. Therefore, it is concluded that increase in NT-3 production is one of the mechanisms by which GV-EA can activate the intrinsic growth ability of spinal neurons after SCI. The experimental results have reinforced the theoretical basis of GV-EA for its clinical efficacy in patients with SCI.
科研通智能强力驱动
Strongly Powered by AbleSci AI