Inflammation in acute CNS injury: a focus on the role of substance P. (12th May 2015)

• Record Type: Journal Article
• Authors: Corrigan, F; Vink, R; Turner, R J
• Other Names: Stewart AG guestEditor.; Beart PM guestEditor.
• Is Part Of: British journal of pharmacology. Volume 173:Number 4(2016:Feb.)
• Page Start: 703
• Page End: 715
• Publication Date: 2015-05-12
• Subjects: Pharmacology -- Periodicals; Chemotherapy -- Periodicals; Drug Therapy -- Periodicals; Pharmacology -- Periodicals; 615.1
• DOI: 10.1111/bph.13155
• Languages: English
• ISSNs: 0007-1188

Abstract

Abstract : Recently, a number of reports have shown that neurogenic inflammation may play a role in the secondary injury response following acute injury to the CNS, including traumatic brain injury (TBI) and stroke. In particular substance P (SP) release appears to be critically involved. Specifically, the expression of the neuropeptide SP is increased in acute CNS injury, with the magnitude of SP release being related to both the frequency and magnitude of the insult. SP release is associated with an increase in blood–brain barrier permeability and the development of vasogenic oedema as well as neuronal injury and worse functional outcome. Moreover, inhibiting the actions of SP through use of a NK1 receptor antagonist is highly beneficial in both focal and diffuse models of TBI, as well as in ischaemic stroke, with a therapeutic window of up to 12 h. We propose that NK1 receptor antagonists represent a novel therapeutic option for treatment of neurogenic inflammation following acute CNS injury. Linked Articles: This article is part of a themed section on Inflammation: maladies, models, mechanisms and molecules. To view the other articles in this section visithttp://dx.doi.org/10.1111/bph.2016.173.issue-4