Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/95730
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Type: | Journal article |
Title: | NK1 receptor blockade is ineffective in improving outcome following a balloon compression model of spinal cord injury |
Author: | Leonard, A. Thornton, E. Vink, R. |
Citation: | PLoS One, 2014; 9(5):e98364-1-e98364-15 |
Publisher: | Public Library of Science |
Issue Date: | 2014 |
ISSN: | 1932-6203 1932-6203 |
Editor: | Rameshwar, P. |
Statement of Responsibility: | Anna Victoria Leonard, Emma Thornton, Robert Vink |
Abstract: | The neuropeptide substance P (SP) is a well-known mediator of neurogenic inflammation following a variety of CNS disorders. Indeed, inhibition of SP through antagonism of its receptor, the tachykinin NK1 receptor, has been shown to be beneficial following both traumatic brain injury and stroke. Such studies demonstrated that administration of an NK1 receptor antagonist reduced blood-brain-barrier permeability, edema development and improved functional outcome. Furthermore, our recent studies have demonstrated a potential role for SP in mediating neurogenic inflammation following traumatic spinal cord injury (SCI). Accordingly, the present study investigates whether inhibition of SP may similarly play a neuroprotective role following traumatic SCI. A closed balloon compression injury was induced at T10 in New Zealand White rabbits. At 30 minutes post-injury an NK1 receptor antagonist was administered intravenously. Animals were thereafter assessed for blood spinal cord barrier (BSCB) permeability, spinal water content (edema), intrathecal pressure (ITP), and histological and functional outcome from 5 hours to 2 weeks post-SCI. Administration of an NK1 receptor antagonist was not effective in reducing BSCB permeability, edema, ITP, or functional deficits following SCI. We conclude that SP mediated neurogenic inflammation does not seem to play a major role in BSCB disruption, edema development and consequential tissue damage seen in acute traumatic SCI. Rather it is likely that the severe primary insult and subsequent hemorrhage may be the key contributing factors to ongoing SCI injury. |
Keywords: | Blood-Brain Barrier Animals Rabbits Spinal Cord Compression Disease Models, Animal Inflammation Tryptophan Substance P Receptors, Neurokinin-1 Protease Inhibitors Neurokinin-1 Receptor Antagonists |
Rights: | © 2014 Leonard et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
DOI: | 10.1371/journal.pone.0098364 |
Published version: | http://dx.doi.org/10.1371/journal.pone.0098364 |
Appears in Collections: | Aurora harvest 3 Medicine publications |
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hdl_95730.pdf | Published version | 18.07 MB | Adobe PDF | View/Open |
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