Inhibition of sympathetic sprouting in CCD rats by lacosamide

2018 ◽  
Vol 22 (9) ◽  
pp. 1641-1650 ◽  
Author(s):  
Y. Wang ◽  
F. Huo
2011 ◽  
Vol 140 (5) ◽  
pp. S-537
Author(s):  
Chun-Mei Xia ◽  
Denis G. Colomb ◽  
Hamid I. Akbarali ◽  
Li-Ya Qiao

Neuroreport ◽  
2001 ◽  
Vol 12 (16) ◽  
pp. 3529-3532 ◽  
Author(s):  
Hee Jin Kim ◽  
Heung Sik Na ◽  
Seung Keun Back ◽  
Seung Kil Hong

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Pei Liu ◽  
Qing Zhang ◽  
You-shui Gao ◽  
Yi-Gang Huang ◽  
Junjie Gao ◽  
...  

Background. Sympathetic sprouting in the dorsal root ganglion (DRG) following nerve injuries had been proved to induce adult neuropathic pain. However, it is unclear whether the abnormal sprouting occurs in infant nerve injury. Methods. L5 spinal nerve ligation (SNL) or sham surgery was performed on adult rats and 10-day-old pups, and mechanical thresholds and heat hyperalgesia were analyzed on 3, 7, 14, 28, and 56 postoperative days. Tyrosine hydroxylase-labeled sympathetic fibers were observed at each time point, and 2 neurotrophin receptors (p75NTR and TrkA) were identified to explore the mechanisms of sympathetic sprouting. Results. Adult rats rapidly developed mechanical and heat hyperalgesia from postoperative day 3, with concurrent sympathetic sprouting in DRG. In contrast, the pup rats did not show a significantly lower mechanical threshold until postoperative day 28, at which time the sympathetic sprouting became evident in the DRG. No heat hyperalgesia was presented in pup rats at any time point. There was a late expression of glial p75NTR in DRG of pups from postoperative day 28, which was parallel to the occurrence of sympathetic sprouting. The expression of TrkA did not show such a postoperative syncing change. Conclusion. The delayed-onset mechanical allodynia in the infant nerve lesion was accompanied with parallel sympathetic sprouting in DRG. The late parallel expression of glial p75NTR injury may play an essential role in this process, which provides novel insight into the treatment of delayed adolescent neuropathic pain.


2007 ◽  
Vol 107 (3) ◽  
pp. 469-477 ◽  
Author(s):  
Huiqing Li ◽  
Wenrui Xie ◽  
Judith A. Strong ◽  
Jun-Ming Zhang

Background Chronic pain models are commonly defined as either nerve-injury or inflammation models, but recent work suggests inflammatory processes are important in nerve injury-induced pain. Methods In the rat spinal nerve ligation model, the authors examined effects of systemic corticosteroid triamcinolone acetonide (TA) on the cytokine protein profile and sympathetic sprouting in the axotomized sensory ganglia, excitability of sensory neurons, and mechanical sensitivity. Results By postoperative day 3, marked increases (5- to 16-fold) in monocyte chemoattractant protein-1, growth-related oncogene (GRO/KC or CXCL1), and interleukin (IL)-6 were observed, whereas IL-4 and IL-2 levels fell more than fourfold. The increased cytokines and number of sympathetic basket formations in the sensory ganglia were reduced toward normal values by TA given starting at the time of injury. Interleukin-4 and IL-2 levels were not restored by TA. Systemic TA also reduced the firing rate and incidence of bursting activity, but not the overall incidence of spontaneous activity, in large- and medium-sized neurons. Mechanical hypersensitivity on postoperative day 3 was reduced by TA, and some effect could still be observed 4 days after cessation of TA. However, starting TA at day 7 was ineffective. Conclusions Several components of the spinal nerve injury model are responsive to corticosteroid, suggesting inflammatory processes are important in the development of neuropathic pain. The observation that TA was effective when given starting at the time of injury suggests that steroid treatment might alter the development of chronic pain after surgical procedures that involve nerve injury, such as amputation or hernia repair.


2008 ◽  
Vol 45 (5) ◽  
pp. 694-702 ◽  
Author(s):  
Viviane El-Helou ◽  
Pauline C. Beguin ◽  
John Assimakopoulos ◽  
Robert Clement ◽  
Hugues Gosselin ◽  
...  

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