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Leonard A.V.,University of Adelaide | Manavis J.,Hanson Institute Center for Neurological Diseases Pathology | Blumbergs P.C.,University of Adelaide | Blumbergs P.C.,Hanson Institute Center for Neurological Diseases Pathology | Vink R.,University of Adelaide
Spinal Cord | Year: 2014

Study design:An immunohistological assessment of substance P (SP), its NK1 receptor and claudin-5 in human spinal cord injury (SCI) tissue.Objective:To determine whether SP and NK1 receptor immunoreactivity are altered following human traumatic SCI.Setting:Australia.Summary of background data:SP has been implicated in the development of neurogenic inflammation and subsequent edema development following both traumatic brain injury and ischemic stroke. In these conditions, inhibition of its NK1 receptor has been shown to be neuroprotective as reflected in a reduction of edema and improved functional outcome. However, the role of SP following human SCI has not yet been assessed.Methods:Archived human SCI tissue was grouped according to survival times: control (no injury; n=5); immediate (death within an hour of the incident; n=6); 2-5 h (n=3); 3 days (n=5); 1 week (n=3); and 3-4 weeks (n=6). Sections were assessed for SP, its NK1 receptor and claudin-5 using immunohistochemical techniques.Results: Following SCI, dorsal horn SP immunoreactivity demonstrated a profound decrease compared with control tissue, indicating the loss of SP with SCI. A marked increase in perivascular NK1 staining was demonstrated after SCI compared with control levels. No obvious change in claudin-5 immunoreactivity was present immediately following injury, however, by 1 week post-SCI, decreased levels were noted.Conclusion:This study demonstrates that severe acute traumatic human SCI results in decreased SP and an immediate increase in NK1 receptor immunoreactivity, suggesting that there is a neurogenic inflammatory component following human SCI. © 2014 International Spinal Cord Society All rights reserved. Source

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