Delayed sympathetic dependence in the spared nerve injury (SNI) model of neuropathic pain

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Delayed sympathetic dependence in the spared nerve injury (SNI) model of neuropathic pain

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dc.contributor.author Pertin, Marie
dc.contributor.author Allchorne, Andrew J
dc.contributor.author Beggah, Ahmed T
dc.contributor.author Decosterd, Isabelle
dc.contributor.author Woolf, Clifford
dc.date.accessioned 2011-04-24T21:53:15Z
dc.date.issued 2007
dc.identifier.citation Pertin, Marie, Andrew J. Allchorne, Ahmed T. Beggah, Clifford J. Woolf, and Isabelle Decosterd. 2007. Delayed sympathetic dependence in the spared nerve injury (SNI) model of neuropathic pain. Molecular Pain 3: 21. en_US
dc.identifier.issn 1744-8069 en_US
dc.identifier.uri http://nrs.harvard.edu/urn-3:HUL.InstRepos:4874837
dc.description.abstract Background: Clinical and experimental studies of neuropathic pain support the hypothesis that a functional coupling between postganglionic sympathetic efferent and sensory afferent fibers contributes to the pain. We investigated whether neuropathic pain-related behavior in the spared nerve injury (SNI) rat model is dependent on the sympathetic nervous system. Results: Permanent chemical sympathectomy was achieved by daily injection of guanethidine (50 mg/kg s.c.) from age P8 to P21. SNI was performed at adulthood followed by 11 weeks of mechanical and thermal hypersensitivity testing. A significant but limited effect of the sympathectomy on SNI-induced pain sensitivity was observed. The effect was delayed and restricted to cold allodynia-like behavior: SNI-related cold scores were lower in the sympathectomized group compared to the control group at 8 and 11 weeks after the nerve injury but not before. Mechanical hypersensitivity tests (pinprick and von Frey hair threshold tests) showed no difference between groups during the study period. Concomitantly, pericellular tyrosine-hydroxylase immunoreactive basket structures were observed around dorsal root ganglia (DRG) neurons 8 weeks after SNI, but were absent at earlier time points after SNI and in sham operated controls. Conclusion: These results suggest that the early establishment of neuropathic pain-related behavior after distal nerve injury such as in the SNI model is mechanistically independent of the sympathetic system, whereas the system contributes to the maintenance, albeit after a delay of many weeks, of response to cold-related stimuli. en_US
dc.language.iso en_US en_US
dc.publisher BioMed Central en_US
dc.relation.isversionof doi:10.1186/1744-8069-3-21 en_US
dc.relation.hasversion http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1950869/pdf/ en_US
dash.license LAA
dc.title Delayed sympathetic dependence in the spared nerve injury (SNI) model of neuropathic pain en_US
dc.type Journal Article en_US
dc.description.version Version of Record en_US
dc.relation.journal Molecular Pain en_US
dash.depositing.author Woolf, Clifford
dc.date.available 2011-04-24T21:53:15Z
dash.affiliation.other HMS^Neurology-Children's Hospital en_US
dash.affiliation.other HMS^Neurobiology en_US

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