NGF and neuropathic pain: Previously, Djouhri and collaborators have shown that in vivo, L5 DRG neurons after SNL, axotomized, disconnected from their peripheral targets and degenerating, are less likely to make a significant contribution to peripheral pain pathogenesis, while intact L4 DRG neurons, which become hyperexcitable after SNL, possibly due to an overabundance of pro-inflammatory mediators and NGF diffused locally, are more responsible for the enhanced afferent input necessary for initiating and/or maintaining traumatic neuropathic pain [45].