Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/81513
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Type: Journal article
Title: Substance P as a mediator of neurogenic inflammation after balloon compression induced spinal cord injury
Author: Leonard, A.
Thornton, E.
Vink, R.
Citation: Journal of Neurotrauma, 2013; 30(21):1812-1823
Publisher: Mary Ann Liebert Inc Publ
Issue Date: 2013
ISSN: 0897-7151
1557-9042
Statement of
Responsibility: 
Anna V. Leonard, Emma Thornton, and Robert Vink
Abstract: Although clinical spinal cord injury (SCI) occurs within a closed environment, most experimental models of SCI create an open injury. Such an open environment precludes the measurement of intrathecal pressure (ITP), whose increase after SCI has been linked to the development of greater tissue damage and functional deficits. Raised ITP may be potentiated by edema, which we have recently shown to be associated with substance P (SP) induced neurogenic inflammation in both traumatic brain injury and stroke. The present study investigates whether SP plays a similar role as a mediator of neurogenic inflammation after SCI. A closed balloon compression injury was induced at T10 in New Zealand white rabbits. Animals were thereafter assessed for blood spinal cord barrier (BSCB) permeability, edema, ITP, histological outcome, and functional outcome from 5 h to 2 weeks post-SCI. The balloon compression model produced significant increases in BSCB permeability, edema, and ITP along with significant functional deficits that persisted for 2 weeks. Histological assessment demonstrated decreased SP immunoreactivity in the injured spinal cord while NK1 receptor immunoreactivity initially increased before returning to sham levels. In addition, aquaporin 4 immunoreactivity increased early post-SCI, implicating this water channel in the development of edema after SCI. The changes described in the present study support a role for SP as a mediator of neurogenic inflammation after SCI.
Keywords: blood spinal cord barrier; edema; neurogenic inflammation; spinal cord injury; substance P
Rights: © Mary Ann Liebert, Inc.
RMID: 0020132496
DOI: 10.1089/neu.2013.2993
Appears in Collections:Medical Sciences publications

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