text: While we made efforts to profile the loss of several molecularly 
  discrete sensory neuron populations, we acknowledge that not all 
  subtypes were profiled. Furthermore, recent single-cell RNA 
  sequencing has given us a more granular appreciation of the 
  heterogeneity of sensory neurons.42 Future studies could 
  leverage our experimental approach and new transgenic lines 
  to characterize the loss of neurons in more detail. Such 
  experiments may be pertinent before embarking on molecular 
  or functional profiling of populations post–nerve injury. 
  
  Rodents develop marked mechanical and thermal hypersen- 
  sitivity rapidly following nerve injury and before timepoints at 
  which neuron loss is observed.10 This lack of a temporal 
  correlation may suggest a limited contribution to evoked hyper- 
  sensitivities. The temporal profile of ongoing tonic pain (eg, pain 
  aversiveness as measured by condition place preference 
  assays26) is less defined and so is its correlation to the timing of 
  neuron loss. 
  
  4.5. Conclusions 
  
  In sum, we have provided data from multiple complementary 
  experimental approaches to support the hypothesis that DRG 
  neurons are lost following nerve injury in mice. We describe 
  a substantial loss, which is biased towards specific subpopula- 
  tions and particularly present in small-diameter nonpeptidergic 
  nociceptive neurons. 