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Cellular sources of cyclooxygenase‐1 and ‐2 up‐regulation in the spinal dorsal horn after spinal nerve ligation
Author(s) -
Lau Yee Man,
Wong Shing Chau,
Tsang Sin Wah,
Lau Wai Kit,
Lu Ai Ping,
Zhang HongQi
Publication year - 2014
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/nan.12078
Subject(s) - neuropathic pain , microglia , medicine , spinal cord , allodynia , nerve injury , central nervous system , pathogenesis , neuroscience , stimulation , cyclooxygenase , pathology , nociception , hyperalgesia , anesthesia , biology , inflammation , receptor , biochemistry , enzyme
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 L 5 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.