The contribution of TRPM8 and TRPA1 channels to cold allodynia and neuropathic pain.
Cold 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 inves...
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2009-01-01
|
| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC2753652?pdf=render |
| _version_ | 1819236885110718464 |
|---|---|
| author | Ombretta Caspani Sandra Zurborg Dominika Labuz Paul A Heppenstall |
| author_facet | Ombretta Caspani Sandra Zurborg Dominika Labuz Paul A Heppenstall |
| author_sort | Ombretta Caspani |
| collection | DOAJ |
| description | Cold 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. |
| first_indexed | 2024-12-23T13:11:32Z |
| format | Article |
| id | doaj.art-1389b9da398f4557a96b68ba38da16ce |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-23T13:11:32Z |
| publishDate | 2009-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-1389b9da398f4557a96b68ba38da16ce2022-12-21T17:45:43ZengPublic Library of Science (PLoS)PLoS ONE1932-62032009-01-01410e738310.1371/journal.pone.0007383The contribution of TRPM8 and TRPA1 channels to cold allodynia and neuropathic pain.Ombretta CaspaniSandra ZurborgDominika LabuzPaul A HeppenstallCold 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.http://europepmc.org/articles/PMC2753652?pdf=render |
| spellingShingle | Ombretta Caspani Sandra Zurborg Dominika Labuz Paul A Heppenstall The contribution of TRPM8 and TRPA1 channels to cold allodynia and neuropathic pain. PLoS ONE |
| title | The contribution of TRPM8 and TRPA1 channels to cold allodynia and neuropathic pain. |
| title_full | The contribution of TRPM8 and TRPA1 channels to cold allodynia and neuropathic pain. |
| title_fullStr | The contribution of TRPM8 and TRPA1 channels to cold allodynia and neuropathic pain. |
| title_full_unstemmed | The contribution of TRPM8 and TRPA1 channels to cold allodynia and neuropathic pain. |
| title_short | The contribution of TRPM8 and TRPA1 channels to cold allodynia and neuropathic pain. |
| title_sort | contribution of trpm8 and trpa1 channels to cold allodynia and neuropathic pain |
| url | http://europepmc.org/articles/PMC2753652?pdf=render |
| work_keys_str_mv | AT ombrettacaspani thecontributionoftrpm8andtrpa1channelstocoldallodyniaandneuropathicpain AT sandrazurborg thecontributionoftrpm8andtrpa1channelstocoldallodyniaandneuropathicpain AT dominikalabuz thecontributionoftrpm8andtrpa1channelstocoldallodyniaandneuropathicpain AT paulaheppenstall thecontributionoftrpm8andtrpa1channelstocoldallodyniaandneuropathicpain AT ombrettacaspani contributionoftrpm8andtrpa1channelstocoldallodyniaandneuropathicpain AT sandrazurborg contributionoftrpm8andtrpa1channelstocoldallodyniaandneuropathicpain AT dominikalabuz contributionoftrpm8andtrpa1channelstocoldallodyniaandneuropathicpain AT paulaheppenstall contributionoftrpm8andtrpa1channelstocoldallodyniaandneuropathicpain |