text: SNI-related gene expression signatures were less evident in 
  Mrgprd-expressing and C-LTMR neurons at later timepoints, 
  compared with other populations in injured DRG.3 This could be 
  explained by a loss of axotomized neurons of these classes and 
  therefore sampling of only uninjured neurons at 
  this time- 
  point.24,43,64 In terms of the transcriptional response to injury, 
  individual 
  nonpeptidergic nociceptors show enrichment of 
  proapoptotic factors early after injury,23,68 and we extend these 
  results in this study, by describing a subpopulation-specific 
  enrichment of GO terms associated with apoptosis that is evident 
  as early as 3 days after 
  injury. Such data and single-cell 
  transcriptomic profiling of all DRG neurons following injury37,44 
  may offer the opportunity to elucidate the cell death pathways 
  engaged and upstream effectors that enrich this process to 
  nonpeptidergic nociceptive neurons. 
  
  platform to help delineate the precise cell death pathways and 
  signaling cascades engaged (which could then be experimentally 
  manipulated). Such studies should consider that plasticity may 
  evolve over time. The loss of IB41 central terminals is transient 
  following crush and has even been observed to reverse at longer 
  timepoints following SNItrans.36 These observations, in conjunction 
  with ours of loss of neurons, raise the intriguing question of the 
  source of such central reinnervation. 