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Differential activation of C1 complement components in rat spinal cord after sciatic nerve injury
Author(s) -
Mika J.,
Przewłocka B.,
Stover C.,
Schwaeble W. J.,
Weihe E.,
Schäfer M. K.H.
Publication year - 2003
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.85.s2.20_5.x
Subject(s) - microglia , neuropathic pain , lesion , spinal cord , sciatic nerve , neuroscience , medicine , complement system , complement c1q , spinal cord injury , sciatic nerve injury , central nervous system , allodynia , lumbar spinal cord , inflammation , anesthesia , pathology , nociception , biology , hyperalgesia , immunology , receptor , antibody
Neuroimmune interactions are discussed to drive neuropathic pain. We used the Bennett model to correlate pain and cellular expression profiles of the complement factors C1q and C1q‐associated serine proteases C1r/C1s in lumbar spinal cord. At 2 days C1q mRNA levels increased ipsilateral to the lesion, and peaked at 8 days when allodynia and severe walking problems were present. During regeneration walking problems disappeared together with C1q mRNA levels. C1q biosynthesis was restricted to microglia. Surprisingly, C1s/C1r biosynthesis was not increased after injury suggesting a role for C1q different from classical complement activation. Sustained C1q expression in spinal microglia after lesion in conjunction with pain behavior indicates that microglial C1q may be causally involved in the development and maintenance of neuropathic pain. Acknowledgements: Supported by BMBF01GG9818, SFB297, DFGWE910/8‐3, KBN3P05C00623.