Involvement of peripheral NFκB in tetanic sciatic stimulation-induced neuropathic pain.
- Author:
Zhe-Chen WANG
1
;
Ning LÜ
;
Yu-Qiu ZHANG
Author Information
1. Institute of Neurobiology, Fudan University, Shanghai 200032, China. yuqiuzhang@fudan.edu.cn.
- Publication Type:Journal Article
- MeSH:
Animals;
Ganglia, Spinal;
metabolism;
Hyperalgesia;
physiopathology;
Long-Term Potentiation;
NF-kappa B;
metabolism;
Neuroglia;
metabolism;
Pain Measurement;
Rats;
Rats, Sprague-Dawley;
Schwann Cells;
metabolism;
Sciatic Neuropathy;
physiopathology;
Signal Transduction;
Spinal Cord;
metabolism
- From:
Acta Physiologica Sinica
2013;65(5):489-496
- CountryChina
- Language:Chinese
-
Abstract:
Tetanic stimulation of the sciatic nerve (TSS) induces long-term potentiation (LTP) of both C- and A-fiber-evoked field potentials in the spinal dorsal horn and long-lasting mechanical allodynia in rats. Though central mechanisms underlying those phenomena have been well studied, peripheral mechanisms still remain poorly known. Nuclear factor kappa B (NFκB) is an important transcription factor. In the spinal cord, NFκB plays a key role in regulating the expression of numerous pro-inflammation factors and contributes to glial activation in central nervous system, suggesting the involvement of spinal NFκB in central sensitization. To address whether NFκB in the dorsal root ganglion (DRG) participates in peripheral sensitization, we examined NFκB expression in the DRG and the effect of inhibiting NFκB activation on neuropathic pain using behavior test, Western blot analysis and immunohistochemical approaches. The results showed that TSS induced long-lasting mechanical allodynia in bilateral hind paws and increased phospho-NFκB expression in the bilateral DRG. The activated NFκB mainly expressed in nuclei not only of neurons, but also of Schwann cells and satellite glial cells. Moreover, NFκB inhibitor pyrrolidine dithiocarbamate (PDTC) significantly alleviated TSS-induced allodynia. Our results suggest that peripheral NFκB may be involved in TSS-induced neuropathic pain, and provide new evidence for the peripheral mechanism of 'mirror pain'.
