Cellular sources of cyclooxygenase-1 and -2 up-regulation in the spinal dorsal horn after spinal nerve ligation
Version of Record online: 22 APR 2014
© 2013 British Neuropathological Society
Neuropathology and Applied Neurobiology
Volume 40, Issue 4, pages 452–463, June 2014
How to Cite
Lau, Y. M., Wong, S. C., Tsang, S. W., Lau, W. K., Lu, A. P. and Zhang, H. (2014), Cellular sources of cyclooxygenase-1 and -2 up-regulation in the spinal dorsal horn after spinal nerve ligation. Neuropathology and Applied Neurobiology, 40: 452–463. doi: 10.1111/nan.12078
- Issue online: 22 APR 2014
- Version of Record online: 22 APR 2014
- Accepted manuscript online: 31 JUL 2013 02:46AM EST
- Manuscript Accepted: 29 JUL 2013
- Manuscript Received: 4 JAN 2013
- Hong Kong Baptist University. Grant Numbers: FRG05-06/II-55, FRG/04-05/I-16
- neuropathic pain;
- spinal cord
Recent studies suggested that the development of neuropathic pain associated with neural injury may be partly due to up-regulation of cyclooxygenase (COX) in the central nervous system. However, the cellular sources of COX-1 and COX-2 up-regulation following nerve injury are unclear.
We investigated the spinal cellular sources of COX-1 and COX-2 in association with allodynia following L5 spinal nerve ligation (SNL).
Post-SNL pain-related behaviour was shown by increased sensitivity to mechanical stimulation. There was a significant increase in both COX-1 and COX-2 immunoreactivity (P < 0.01) on the ipsilateral side of spinal dorsal horn. Double immunofluorescence labelling demonstrated that COX-1 immunoreactive cells colocalized chiefly with dorsal horn neuronal nuclei and microglia, whereas COX-2 was expressed in neuronal cytoplasm.
These findings demonstrate that while spinal dorsal horn neurones are important source of COX-1 and COX-2 after nerve injury, microglia also contribute to the pathogenesis of neuropathic pain, partly by producing additional COX-1.