Alterations in the BDNF–mTOR Signaling Pathway in the Spinal Cord Contribute to Hyperalgesia in a Rodent Model of Chronic Restraint Stress

Neuroscience ◽  
2019 ◽  
Vol 409 ◽  
pp. 142-151 ◽  
Author(s):  
Niannian Huang ◽  
Chun Yang ◽  
Dongyu Hua ◽  
Shan Li ◽  
Gaofeng Zhan ◽  
...  
2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Jingying Zhou ◽  
Xue Huo ◽  
Benson O. A. Botchway ◽  
Luyao Xu ◽  
Xiaofang Meng ◽  
...  

Spinal cord injury (SCI) causes a high rate of morbidity and disability. The clinical features of SCI are divided into acute, subacute, and chronic phases according to its pathophysiological events. The mammalian target of rapamycin (mTOR) signaling pathway plays an important role in cell death and inflammation in the acute phase and neuroregeneration in the subacute/chronic phases at different times. Resveratrol has the potential of regulating cell growth, proliferation, metabolism, and angiogenesis through the mTOR signaling pathway. Herein, we explicate the role of resveratrol in the repair of SCI through the inhibition of the mTOR signaling pathway. The inhibition of the mTOR pathway by resveratrol has the potential of serving as a neuronal restorative mechanism following SCI.


2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Ke Li ◽  
Juntong Liu ◽  
Liangyu Song ◽  
Wei Lv ◽  
Xi Tian ◽  
...  

Electroacupuncture (EA) is widely recognized as clinical treatment of spinal cord injury (SCI). The purpose of this study is to elucidate whether and how the PI3K/AKT/mTOR signaling pathway plays any role in EA treating SCI. Rats were randomly divided into four equal groups: Control Group, Sham-operation Group, Model Group, and EA Group, then further randomly divided into the following subgroups: 1-day (n=12), 1-day rapamycin (n=6), 14-day (n=18), and 28-day (n=18). A rat model of SCI was established by a modified Allen’s weight-drop method. In the EA Group, rats were stimulated on Dazhui (GV14) and Mingmen (GV4) for 20 min by sterilized stainless steel needles. In the EA Group, the Basso, Beattie, and Bresnahan locomotor rating scale showed obvious improved locomotor function, and hematoxylin-eosin staining and magnetic resonance imaging showed that the histological morphology change of injured spinal cord tissue was obviously alleviated. Also, blocking spinal mTOR by injection of rapamycin showed that mTOR existed in the injured spinal cord, and EA could significantly activate mTOR in SCI rats. And immunohistochemistry and western blot analysis on the PI3K/AKT/mTOR signaling pathway showed that levels of PI3K, AKT, mTOR, and p70S6K in the injured spinal cord tissue were greatly increased in the EA Group, while the levels of PTEN and caspase 3 were decreased. The present study suggests that EA could affect cell growth, apoptosis, and autophagy through the PI3K/AKT/mTOR signaling pathway.


Neuroscience ◽  
2016 ◽  
Vol 329 ◽  
pp. 193-200 ◽  
Author(s):  
Zipeng Zhou ◽  
Shurui Chen ◽  
Haosen Zhao ◽  
Chen Wang ◽  
Kai Gao ◽  
...  

2020 ◽  
Vol 736 ◽  
pp. 135263
Author(s):  
Sen Lin ◽  
He Tian ◽  
Jiaquan Lin ◽  
Chang Xu ◽  
Yajiang Yuan ◽  
...  

2018 ◽  
Vol 43 (5) ◽  
pp. 1111-1117 ◽  
Author(s):  
Yue Guo ◽  
Fang Wang ◽  
Haopeng Li ◽  
Hui Liang ◽  
Yuhuan Li ◽  
...  

Author(s):  
Dayu Pan ◽  
Shibo Zhu ◽  
Weixin Zhang ◽  
Zhijian Wei ◽  
Fuhan Yang ◽  
...  

AbstractSpinal cord injury (SCI) is catastrophic to humans and society. However, there is currently no effective treatment for SCI. Autophagy is known to serve critical roles in both the physiological and pathological processes of the body, but its facilitatory and/or deleterious effects in SCI are yet to be completely elucidated. This study aimed to use primary Schwann cell-derived exosomes (SCDEs) to treat rats after SCI. In the present study, SCDEs were purified and their efficacy in ameliorating the components of SCI was examined. Using both in vivo and in vitro experiments, it was demonstrated that SCDEs increased autophagy and decreased apoptosis after SCI, which promoted axonal protection and the recovery of motor function. Furthermore, it was discovered that an increased number of SCDEs resulted in a decreased expression level of EGFR, which subsequently inhibited the Akt/mTOR signaling pathway, which upregulated the level of autophagy to ultimately induce microtubule acetylation and polymerization. Collectively, the present study identified that SCDEs could induce axonal protection after SCI by increasing autophagy and decreasing apoptosis, and it was suggested that this may involve the EGFR/Akt/mTOR signaling pathway.


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