Document Type

Journal Article

Department/Unit

School of Chinese Medicine

Language

English

Abstract

Aims: 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. Methods: We investigated the spinal cellular sources of COX-1 and COX-2 in association with allodynia following L5 spinal nerve ligation (SNL). Results: 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. Conclusion: 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. © 2013 British Neuropathological Society.

Keywords

Astrocyte, COX, Microglia, Neurone, Neuropathic pain, Spinal cord

Publication Date

6-2014

Source Publication Title

Neuropathology and Applied Neurobiology

Volume

40

Issue

4

Start Page

452

End Page

463

Publisher

Wiley

Peer Reviewed

1

Copyright

This is the peer reviewed version of the following article: 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. Neuropathol Appl Neurobiol, 40: 452–463. doi:10.1111/nan.12078, which has been published in final form at http://dx.doi.org/10.1111/nan.12078. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.

Funder

Supported by Hong Kong Baptist University FRG05-06/ II-55 & FRG/04-05/I-16, and SCM postdoctoral fellowship. We thank Nickie Chan for her invaluable technical support.

DOI

10.1111/nan.12078

Link to Publisher's Edition

http://dx.doi.org/10.1111/nan.12078

ISSN (print)

03051846

ISSN (electronic)

13652990

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