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dc.contributor.authorCorrigan, F.en
dc.contributor.authorVink, R.en
dc.contributor.authorTurner, R.en
dc.identifier.citationBritish Journal of Pharmacology, 2016; 173(4):703-715en
dc.description.abstractRecently, 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.en
dc.description.statementofresponsibilityF Corrigan, R Vink, and R J Turneren
dc.rights© 2015 The British Pharmacological Societyen
dc.subjectCentral Nervous System; Animals; Humans; Inflammation; Substance P; Neurokinin-1 Receptor Antagonistsen
dc.titleInflammation in acute CNS injury: a focus on the role of substance Pen
dc.typeJournal articleen
pubs.library.collectionMedicine publicationsen
dc.identifier.orcidCorrigan, F. [0000-0001-6150-8893]en
dc.identifier.orcidVink, R. [0000-0002-4885-0667]en
dc.identifier.orcidTurner, R. [0000-0003-4278-8302]en
Appears in Collections:Medicine publications

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