Review
Version 1
Preserved in Portico This version is not peer-reviewed
Evidence for the involvement of the Tachykinin NK1 Receptor in Acute Inflammation of the Central Nervous System
Version 1
: Received: 5 September 2023 / Approved: 6 September 2023 / Online: 7 September 2023 (03:59:49 CEST)
A peer-reviewed article of this Preprint also exists.
Turner, R.J.; Nimmo, A.J. Evidence for the Involvement of the Tachykinin NK1 Receptor in Acute Inflammation of the Central Nervous System. Receptors 2023, 2, 232-250. Turner, R.J.; Nimmo, A.J. Evidence for the Involvement of the Tachykinin NK1 Receptor in Acute Inflammation of the Central Nervous System. Receptors 2023, 2, 232-250.
Abstract
Neuroinflammation is considered to be a significant component in a range of neuropathologies. Unfortunately, whilst its role is well recognized, the options for therapeutic intervention are limited. As such, there is a need to identify novel targets in order to increase treatment options. Given its role as both a neurotransmitter and an immune modulator, substance P and its NK1 receptor have been widely studied as a potential therapeutic target. There is evidence that NK1 receptor antagonists may exert beneficial effects in a range of conditions, including traumatic brain injury and stroke. Blocking the NK1 receptor has been shown to reduce blood-brain barrier dysfunction, reduce cerebral oedema, and reduce the levels of pro-inflammatory cytokines. These actions are associated with improved survival and functional outcomes. The NK1 receptor has also been shown to be involved in the inflammatory reaction to CNS infection, and hence antagonist may have some benefit in reducing infection-driven inflammation. However, the NK1 receptor may also play a role in the host immune response to infection, and so here, the potential beneficial and detrimental effects need to be carefully balanced. As such, the purpose of this review is to provide a summary of the involvement of substance P in acute inflammation, particularly in the context of traumatic brain injury and stroke.
Keywords
NK1 receptor; Substance P; Neuroinflammation; Blood-brain barrier; Traumatic brain injury; Stroke; CNS infection; NK1 receptor antagonist
Subject
Medicine and Pharmacology, Neuroscience and Neurology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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