Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680865
Title: An in vitro model for the study of transient receptor potential channels on human sensory neurons
Author: Clarke, Rebecca
ISNI:       0000 0004 5917 4320
Awarding Body: Queen's University Belfast
Current Institution: Queen's University Belfast
Date of Award: 2015
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Abstract:
Sensory neurons are responsible for detecting noxious chemical, mechanical and thermal stimuli and relaying the information to the central nervous system. They also contribute to local neurogenic inflammation via the release of neuropeptides. Sensory neurons express a variety of ion channels, including the transient receptor potential (TRP) channels. TRP channels are one of the main families of ion channels responsible for nociception and are desirable targets for analgesic and anti-inflammatory therapies. TRP channel studies on human sensory neurons has been hampered by the fact that peripheral neurons lack theis cell bodies, which are housed in neuronal ganglia and are inaccessible via peripheral tissue biopsy. To overcome this limitation we have differentiated human dental pulp stem cells towards a neuronal phenotype, termed peripheral neuronal equivalebts (PNEs), which have their cell bodies present. Microfluorimetric and electrophysiological techniques have demonstrated the functional expression of TRP channels on PNEs, specifically TRPA 1 and TRPV1. Therefore PNEs represent a novel source of functional human sensory neurons suitable for in vitro TRP channel studies. In vivo, neuronal TRP channels become hypersensitised in inflammatory and infectious environments however the exact mechanism through which this occurs is unknown. PNEs pre-treated with pro-inflammatory cytokines generated larger responses to TRP channel agonists when compared to untreated PNEs however no alterations in TRP channel gene expression were observed. PNEs infected with human rhinovirus also show no change in TRP channel gene expression suggesting that TRP channel sensitisation, rather than upregulation, contributes to nerve hypersensitivity.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.680865  DOI: Not available
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