SNi公司
神经病理性疼痛
PI3K/AKT/mTOR通路
医学
自噬
脊髓
神经损伤
突触可塑性
长时程增强
伤害
神经科学
内科学
内分泌学
作者
Jijun Hu,Xueling Chen,Jie Cheng,Fanli Kong,Hui Xia,Jiang Wu
出处
期刊:Neuroreport
[Ovid Technologies (Wolters Kluwer)]
日期:2021-06-17
卷期号:32 (11): 925-935
被引量:2
标识
DOI:10.1097/wnr.0000000000001684
摘要
Unveiling the etiology and the underlying mechanism of neuropathic pain, a poorly treated disease, is essential for the development of effective therapies. This study aimed to explore the role of mammalian target of rapamycin (mTOR) signaling in autophagy-mediated neuropathic pain. We established a spared nerve injury (SNI) model in adult male SD rats by ligating the common peroneal nerve and tibial, with the distal end cutoff. The paw withdrawal threshold (PWT) and C/A-fiber evoked field potentials were determined by electrophysiologic tests at day 0 (before operation), day 7 and day 14 postoperation, and SNI significantly increased field potentials (P < 0.05). Immunohistochemistry and western blots using spinal cord tissues showed that the expressions of GluR1, GluR2, Beclin-1, p62, mTOR and 4EBP1 were significantly increased after SNI (all P < 0.05), whereas the expressions of LC3 and LAMP2 were significantly decreased after SNI (all P < 0.05). Rapamycin efficiently counteracted the effect of SNI and restored the phenotypes to the level comparable to the sham control. In conclusion, rapamycin inhibits C/A-fiber-mediated long-term potentiation in the SNI rat model of neuropathic pain, which might be mediated by activation of autophagy signaling and downregulation of GluRs expression.
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