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dc.contributor.authorLyu, Chuangen_US
dc.contributor.authorLyu, Gong-Weien_US
dc.contributor.authorMartinez, Auroraen_US
dc.contributor.authorShi, Tie-Junen_US
dc.date.accessioned2018-02-09T08:56:05Z
dc.date.available2018-02-09T08:56:05Z
dc.date.issued2017-08-30
dc.PublishedLyu C, Lyu G, Martinez A, Shi Sten. Effect of nerve injury on the number of dorsal root ganglion neurons and autotomy behavior in adult Bax-deficient mice. Journal of Pain Research. 2017;10:2079-2087eng
dc.identifier.issn1178-7090
dc.identifier.urihttps://hdl.handle.net/1956/17360
dc.description.abstractBackground: The proapoptotic molecule BAX, plays an important role in mitochondrial apoptotic pathway. Dorsal root ganglion (DRG) neurons depend on neurotrophic factors for survival at early developmental stages. Withdrawal of neurotrophic factors will induce apoptosis in DRG neurons, but this type of cell death can be delayed or prevented in neonatal Bax knockout (KO) mice. In adult animals, evidence also shows that DRG neurons are less dependent upon neurotrophic factors for survival. However, little is known about the effect of Bax deletion on the survival of normal and denervated DRG neurons in adult mice. Methods: A unilateral sciatic nerve transection was performed in adult Bax KO mice and wild-type (WT) littermates. Stereological method was employed to quantify the number of lumbar-5 DRG neurons 1 month post-surgery. Nerve injury-induced autotomy behavior was also examined on days 1, 3, and 7 post-surgery. Results: There were significantly more neurons in contralateral DRGs of KO mice as compared with WT mice. The number of neurons was reduced in ipsilateral DRGs in both KO and WT mice. No changes in size distributions of DRG neuron profiles were detected before or after nerve injury. Injury-induced autotomy behavior developed much earlier and was more serious in KO mice. Conclusion: Although postnatal death or loss of DRG neurons is partially prevented by Bax deletion, this effect cannot interfere with long-term nerve injury-induced neuronal loss. The exaggerated self-amputation behavior observed in the mutant mice indicates that Bax deficiency may enhance the development of spontaneous pain following nerve injury.en_US
dc.language.isoengeng
dc.publisherDove Presseng
dc.rightsAttribution CC BY-NCeng
dc.rights.urihttps://creativecommons.org/licenses/by-nc/3.0/eng
dc.subjectapoptosiseng
dc.subjectaxotomyeng
dc.subjectcell deatheng
dc.subjectchronic paineng
dc.subjectunbiased counting methodeng
dc.subjectsensory neuronseng
dc.titleEffect of nerve injury on the number of dorsal root ganglion neurons and autotomy behavior in adult Bax-deficient miceen_US
dc.typePeer reviewed
dc.typeJournal article
dc.date.updated2018-01-03T09:22:07Z
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2017 The Author(s)
dc.identifier.doihttps://doi.org/10.2147/jpr.s133087
dc.identifier.cristin1495211
dc.source.journalJournal of Pain Research


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