Inhibition of calcineurin inhibits the desensitization of capsaicin-evoked currents in cultured dorsal root ganglion neurones from adult rats

1996 ◽  
Vol 431 (S6) ◽  
pp. 828-837 ◽  
Author(s):  
R. J. Docherty ◽  
J. C. Yeats ◽  
S. Bevan ◽  
H. W. G. M. Boddeke
2015 ◽  
Vol 23 ◽  
pp. S218
Author(s):  
Quinn H. Hogan ◽  
Gregory Fischer ◽  
Dean Caron ◽  
Hongwei Yu

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.


2001 ◽  
Vol 285 (5) ◽  
pp. 1114-1120 ◽  
Author(s):  
Su-Yong Eun ◽  
Sung Jun Jung ◽  
Yun Kyung Park ◽  
Jiyeon Kwak ◽  
Sang Jeong Kim ◽  
...  

Endocrinology ◽  
2008 ◽  
Vol 149 (7) ◽  
pp. 3452-3460 ◽  
Author(s):  
Anuradha Chakrabarty ◽  
Audrey Blacklock ◽  
Stanislav Svojanovsky ◽  
Peter G. Smith

Many painful conditions occur more frequently in women, and estrogen is a predisposing factor. Estrogen may contribute to some pain syndromes by enhancing axon outgrowth by sensory dorsal root ganglion (DRG) neurons. The objective of the present study was to define mechanisms by which estrogen elicits axon sprouting. The estrogen receptor-α agonist propyl pyrazole triol induced neurite outgrowth from cultured neonatal DRG neurons, whereas the estrogen receptor-β agonist diarylpropionitrile was ineffective. 17β-Estradiol (E2) elicited sprouting from peripherin-positive unmyelinated neurons, but not larger NF200-positive myelinated neurons. Microarray analysis showed that E2 up-regulates angiotensin II (ANGII) receptor type 2 (AT2) mRNA in vitro, and studies in adult rats confirmed increased DRG mRNA and protein in vivo. AT2 plays a central role in E2-induced axon sprouting because AT2 blockade by PD123,319 eliminated estrogen-mediated sprouting in vitro. We assessed whether AT2 may be responding to locally synthesized ANGII. DRG from adult rats expressed mRNA for renin, angiotensinogen, and angiotensin converting enzyme (ACE), and protein products were present and occasionally colocalized within neurons and other DRG cells. We determined if locally synthesized ANGII plays a role in estrogen-mediated sprouting by blocking its formation using the ACE inhibitor enalapril. ACE inhibition prevented estrogen-induced neuritogenesis. These findings support the hypothesis that estrogen promotes DRG nociceptor axon sprouting by up-regulating the AT2 receptor, and that locally synthesized ANGII can induce axon formation. Therefore, estrogen may contribute to some pain syndromes by enhancing the pro-neuritogenic effects of AT2 activation by ANGII.


2018 ◽  
Vol 301 (5) ◽  
pp. 849-861 ◽  
Author(s):  
Ana Leda Bertoncini Simões ◽  
Greice Anne Rodrigues Silva ◽  
Carolina Giorgetto ◽  
Elisabete de Cassia do Carmo-Campos ◽  
Fernando José Dias ◽  
...  

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