Effect of touch-stimulus on the expression of C-fos and TrkA in spinal cord following chronic constriction injury of the sciatic nerve in rats

Author(s):  
Wan Li ◽  
Luo Ailin ◽  
Yu Honghui ◽  
Tian Yuke
2008 ◽  
Vol 107 (6) ◽  
pp. 1741-1752 ◽  
Author(s):  
D. Gómez-Nicola ◽  
B. Valle-Argos ◽  
M. Suardíaz ◽  
J. S. Taylor ◽  
M. Nieto-Sampedro

2013 ◽  
Vol 110 (7) ◽  
pp. 1663-1671 ◽  
Author(s):  
Hongmei Zhang ◽  
Haijun Zhang ◽  
Patrick M. Dougherty

Nerve injury-induced central sensitization can manifest as an increase in excitatory synaptic transmission and/or as a decrease in inhibitory synaptic transmission in spinal dorsal horn neurons. Cytokines such as tumor necrosis factor-α (TNF-α) are induced in the spinal cord under various injury conditions and contribute to neuropathic pain. In this study we examined the effect of TNF-α in modulating excitatory and inhibitory synaptic input to spinal substantia gelatinosa (SG) neurons over time in mice following chronic constriction injury (CCI) of the sciatic nerve. Whole cell patch-clamp studies from SG neurons showed that TNF-α enhanced overall excitability of the spinal cord early in time following nerve injury 3 days after CCI compared with that in sham control mice. In contrast, the effects of TNF were blunted 14 days after CCI in nerve-injured mice compared with sham surgery mice. Immunohistochemical staining showed that the expression of TNF-α receptor 1 (TNFR1) was increased at 3 days but decreased at 14 days following CCI in the ipsilateral vs. the contralateral spinal cord dorsal horn. These results suggest that TNF-α acting at TNFR1 is important in the development of neuropathic pain by facilitating excitatory synaptic signaling in the acute phases after nerve injury but has a reduced effect on spinal neuron signaling in the later phases of nerve injury-induced pain. Failure of the facilatory effects of TNF-α on excitatory synaptic signaling in the dorsal horn to resolve following nerve injury may be an important component in the transition between acute and chronic pain conditions.


2020 ◽  
Vol 10 (10) ◽  
pp. 731
Author(s):  
Muhammad Faheem ◽  
Syed Hussain Ali ◽  
Abdul Waheed Khan ◽  
Mahboob Alam ◽  
Umair Ilyas ◽  
...  

The production and up-regulation of inflammatory mediators are contributing factors for the development and maintenance of neuropathic pain. In the present study, the post-treatment of synthetic 1,3,4 oxadiazole derivative (B3) for its neuroprotective potential in chronic constriction injury-induced neuropathic pain was applied. In-silico studies were carried out through Auto Dock, PyRx, and DSV to obtain the possible binding and interactions of the ligands (B3) with COX-2, IL-6, and iNOS. The sciatic nerve of the anesthetized rat was constricted with sutures 3/0. Treatment with 1,3,4-oxadiazole derivative was started a day after surgery and continued until the 14th day. All behavioral studies were executed on day 0, 3rd, 7th, 10th, and 14th. The sciatic nerve and spinal cord were collected for further molecular analysis. The interactions in the form of hydrogen bonding stabilizes the ligand target complex. B3 showed three hydrogen bonds with IL-6. B3, in addition to correcting paw posture/deformation induced by CCI, attenuates hyperalgesia (p < 0.001) and allodynia (p < 0.001). B3 significantly raised the level of GST and GSH in both the sciatic nerve and spinal cord and reduced the LPO and iNOS (p < 0.001). B3 attenuates the pathological changes induced by nerve injury, which was confirmed by H&E staining and IHC examination. B3 down-regulates the over-expression of the inflammatory mediator IL-6 and hence provides neuroprotective effects in CCI-induced pain. The results demonstrate that B3 possess anti-nociceptive and anti-hyperalgesic effects and thus minimizes pain perception and inflammation. The possible underlying mechanism for the neuroprotective effect of B3 probably may be mediated through IL-6.


2020 ◽  
Vol 731 ◽  
pp. 135029
Author(s):  
Jenny L. Wilkerson ◽  
Jinmai Jiang ◽  
Jasmine S. Felix ◽  
Julie K. Bray ◽  
Lais da Silva ◽  
...  

Pain Medicine ◽  
2021 ◽  
Author(s):  
Xun Chen ◽  
Jianbo Dai ◽  
Dan Li ◽  
Xingliang Huang ◽  
Cehua Qu

Abstract Objectives The treatment for neuropathic pain is still a big challenge. Pulsed radiofrequency technique has been widely used to relieve neuropathic pain in recent years. The purpose of this study is to optimize the temperature for pulsed radiofrequency therapy. Design Animal, experimental study. Methods Seventy-five male SD rats were randomly divided into five groups: Sham operation group (Sham group), chronic constriction injury group (CCI group), PRF 42°C group (P42 group), PRF 50°C group (P50 group), and PRF 60°C group (P60 group). The hindpaw withdrawal threshold (HWT), paw thermal withdrawal latency (PTWL), sciatic nerve structure, and the concentration of spinal methionine enkephalin(M-ENK) were detected to identify which temperature is the best for PRF treatment. Results PRF at 42°C, 50°C and 60°C significantly alleviated the pain in CCI rats. The therapeutic effects of 50°C and 60°C were similar, and both were better than 42°C. In addition, PRF using 42°C, 50°C, and 60°C mediated nerve injury to sciatic nerve were grade 1, 1, and 2, respectively. The concentration of M-ENK in spinal cord increased accompanying with the increasing of the temperature of PRF. Conclusions PRF using 50°C could induce less damage while achieving better improvement of mechanical and thermal pain threshold than 42°C and 60°C in CCI rats, which may be achieved by promoting the expression of M-ENK in spinal cord.


2011 ◽  
Vol 28 ◽  
pp. 192
Author(s):  
T. Brandenburger ◽  
M. Castoldi ◽  
M. Brendel ◽  
L. Schlösser ◽  
I. Bauer ◽  
...  

2020 ◽  
Vol 10 ◽  
Author(s):  
Samad Nazemi ◽  
Faranak Jafari ◽  
Bahareh Amin ◽  
Omid Gholami ◽  
Marzieh Kafami ◽  
...  

Objective: Although morphine is among of the first line medicines for treatment of neuropathic pain, evidence has shown that the morphine efficacy gradually decreases and a tolerance can occur. Rregarding the many reports concerning the antinociceptive and anti-inflammatory properties of umbelliprenin (UMB), this study aimed to investigate the effect of UMB on antinociceptive activity of morphine in a rat model of neuropathic pain induced by chronic constriction injury (CCI) of the sciatic nerve. Methods: Twenty-four male Wistar rats were randomly divided into sham, CCI and CCI + UMB100 (100 μg UMB per rat) groups. UMB was intrathecally administered once daily for four consecutive days (from the day before surgery until the day 2 after surgery). All the animals received a single dose of morphine (5 mg/kg, s.c.) on day 14. To evaluate the effect of UMB on antinociceptive activity of morphine, allodynia and hyperalgesia were measured using the von-Frey and hot plate tests, before and 30 min after morphine injection, and the Percentage of Maximum Possible Effect (%MPE) was calculated. In addition, the expression and concentration of tumor necrosis factor-alpha (TNF-α), as a proinflammatory cytokine, was measured in the spinal cord using quantitative real-time PCR (RT-PCR) and ELISA, respectively. Key Findings: UMB significantly enhanced anti-allodynic and anti-hyperalgesic effects of morphine in the neuropathic animals. Moreover, UMB considerably downregulated TNF-α expression in the spinal cord of the animals. Conclusion: UMB can enhance antinociceptive effects of morphine, and this action may be due in part to its anti-inflammatory property.


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