Changes in substance P and NK1 receptor immunohistochemistry following human spinal cord injury.
METHODS
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.


METHODS
Australia.


BACKGROUND
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.


CONCLUSIONS
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.
School of Medical Sciences, University of Adelaide, Adelaide, South Australia, Australia.
A V
AV
Leonard
Hanson Institute Centre for Neurological Diseases/SA Pathology, Adelaide, South Australia, Australia.
J
J
Manavis
1] School of Medical Sciences, University of Adelaide, Adelaide, South Australia, Australia [2] Hanson Institute Centre for Neurological Diseases/SA Pathology, Adelaide, South Australia, Australia.
P C
PC
Blumbergs
School of Medical Sciences, University of Adelaide, Adelaide, South Australia, Australia.
R
R
Vink
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000378:metabolism; D002648:Child; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D018040:Receptors, Neurokinin-1 / Q000378:metabolism*; D013119:Spinal Cord Injuries / Q000378:metabolism*; D013373:Substance P / Q000378:metabolism*; D055815:Young Adult
D015415:Biomarkers; D018040:Receptors, Neurokinin-1; D013373:Substance P