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dc.contributor.authorBernal, Laura
dc.contributor.authorCisneros, Elsa
dc.contributor.authorRoza, Carolina
dc.date2021
dc.date.accessioned2021-07-22T10:48:25Z
dc.date.available2021-07-22T10:48:25Z
dc.identifier.citationBernal L, Cisneros E, Roza C. Activation of the regeneration-associated gene STAT3 and functional changes in intact nociceptors after peripheral nerve damage in mice. Eur J Pain. 2021 Apr;25(4):886-901. doi: 10.1002/ejp.1718. Epub 2021 Jan 1. PMID: 33345380.
dc.identifier.issn1090-3801
dc.identifier.urihttps://reunir.unir.net/handle/123456789/11646
dc.descriptionPublicación con el texto completo en acceso restringido
dc.description.abstractBackground: In the context of neuropathic pain, the contribution of regeneration to the development of positive symptoms is not completely understood. Several efforts have been done to described changes in axotomized neurons, however, there is scarce data on changes occurring in intact neurons, despite experimental evidence of functional changes. To address this issue, we analysed by immunohistochemistry the presence of phosphorylated signal transducer and activator of transcription 3 (pSTAT3), an accepted marker of regeneration, within DRGs where axotomized neurons were retrogradely labelled following peripheral nerve injury. Likewise, we have characterized abnormal electrophysiological properties in intact fibres after partial nerve injury. Methods/Results: We showed that induction of pSTAT3 in sensory neurons was similar after partial or total transection of the sciatic nerve and to the same extent within axotomized and non-axotomized neurons. We also examined pSTAT3 presence on non-peptidergic and peptidergic nociceptors. Whereas the percentage of neurons marked by IB4 decrease after injury, the proportion of CGRP neurons did not change, but its expression switched from small- to large-diameter neurons. Besides, the percentage of CGRP+ neurons expressing pSTAT3 increased significantly 2.5-folds after axotomy, preferentially in neurons with large diameters. Electrophysiological recordings showed that after nerve damage, most of the neurons with ectopic spontaneous activity (39/46) were non-axotomized C-fibres with functional receptive fields in the skin far beyond the site of damage. Conclusions: Neuronal regeneration after nerve injury, likely triggered from the site of injury, may explain the abnormal functional properties gained by intact neurons, reinforcing their role in neuropathic pain. Significance: Positive symptoms in patients with peripheral neuropathies correlate to abnormal functioning of different subpopulations of primary afferents. Peripheral nerve damage triggers regenerating programs in the cell bodies of axotomized but also in non-axotomized nociceptors which is in turn, develop abnormal spontaneous and evoked discharges. Therefore, intact nociceptors have a significant role in the development of neuropathic pain due to their hyperexcitable peripheral terminals. Therapeutical targets should focus on inhibiting peripheral hyperexcitability in an attempt to limit peripheral and central sensitization.es_ES
dc.language.isoenges_ES
dc.publisherEuropean journal of pain (United Kingdom)es_ES
dc.relation.ispartofseries;vol. 25, nº 4
dc.relation.urihttps://onlinelibrary.wiley.com/doi/10.1002/ejp.1718es_ES
dc.rightsrestrictedAccesses_ES
dc.subjectgene STAT3es_ES
dc.subjectnociceptorses_ES
dc.subjectperipheral nervees_ES
dc.subjectmicees_ES
dc.subjectScopuses_ES
dc.subjectJCRes_ES
dc.titleActivation of the regeneration-associated gene STAT3 and functional changes in intact nociceptors after peripheral nerve damage in micees_ES
dc.typeArticulo Revista Indexadaes_ES
reunir.tag~ARIes_ES
dc.identifier.doihttps://doi.org/10.1002/ejp.1718


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