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dc.contributor.authorCaspani, Ombretta
dc.contributor.authorZurborg, Sandra
dc.contributor.authorLabuz, Dominika
dc.contributor.authorHeppenstall, Paul A
dc.date.accessioned2017-08-08T11:12:24Z
dc.date.available2017-08-08T11:12:24Z
dc.date.issued2009-10-08
dc.identifier.issn1932-6203
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/265995
dc.description.abstractCold allodynia is a common feature of neuropathic pain however the underlying mechanisms of this enhanced sensitivity to cold are not known. Recently the transient receptor potential (TRP) channels TRPM8 and TRPA1 have been identified and proposed to be molecular sensors for cold. Here we have investigated the expression of TRPM8 and TRPA1 mRNA in the dorsal root ganglia (DRG) and examined the cold sensitivity of peripheral sensory neurons in the chronic construction injury (CCI) model of neuropathic pain in mice.In behavioral experiments, chronic constriction injury (CCI) of the sciatic nerve induced a hypersensitivity to both cold and the TRPM8 agonist menthol that developed 2 days post injury and remained stable for at least 2 weeks. Using quantitative RT-PCR and in situ hybridization we examined the expression of TRPM8 and TRPA1 in DRG. Both channels displayed significantly reduced expression levels after injury with no change in their distribution pattern in identified neuronal subpopulations. Furthermore, in calcium imaging experiments, we detected no alterations in the number of cold or menthol responsive neurons in the DRG, or in the functional properties of cold transduction following injury. Intriguingly however, responses to the TRPA1 agonist mustard oil were strongly reduced.Our results indicate that injured sensory neurons do not develop abnormal cold sensitivity after chronic constriction injury and that alterations in the expression of TRPM8 and TRPA1 are unlikely to contribute directly to the pathogenesis of cold allodynia in this neuropathic pain model.
dc.format.mediumElectronic
dc.languageeng
dc.publisherPublic Library of Science (PLoS)
dc.subjectGanglia, Spinal
dc.subjectAnimals
dc.subjectMice
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectPain
dc.subjectCalcium
dc.subjectMenthol
dc.subjectAnkyrins
dc.subjectCalcium Channels
dc.subjectTemperature
dc.subjectMale
dc.subjectTransient Receptor Potential Channels
dc.subjectTRPC Cation Channels
dc.subjectTRPM Cation Channels
dc.subjectCold Temperature
dc.subjectSensory Receptor Cells
dc.subjectThermosensing
dc.subjectTRPA1 Cation Channel
dc.titleThe contribution of TRPM8 and TRPA1 channels to cold allodynia and neuropathic pain.
dc.typeArticle
prism.issueIdentifier10
prism.publicationDate2009
prism.publicationNamePLoS One
prism.startingPagee7383
prism.volume4
dc.identifier.doi10.17863/CAM.11953
dcterms.dateAccepted2009-09-14
rioxxterms.versionofrecord10.1371/journal.pone.0007383
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2009-10-08
dc.identifier.eissn1932-6203
rioxxterms.typeJournal Article/Review
cam.issuedOnline2009-10-08


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