text: loss of nonpeptidergic 
  nociceptors, we re-analyzed a previous population-specific 
  transcriptomic dataset of mouse DRG neurons following nerve 
  injury for potential upregulation of cell death pathways (Fig. S7, 
  http://links.lww.com/PAIN/C84).3 We found that early after injury 
  (3 days post-SNItrans), nonpeptidergic (MrgDCreERT2-expressing) 
  neurons showed enhanced enrichment of GO terms associated 
  with apoptosis, in contrast to a broad population of nociceptors 
  (labelled with Scn10aCreERT2), peptidergic nociceptors (Calca- 
  CreERT2), C-LTMRs (ThCreERT2), and Ab-RA (rapidly adapting) and 
  Ad-LTMRs (Ad/Ab-LTMR, Ntrk2CreERT2;AdvillinFlpO), 
  in which 
  there was less or no enrichment of cell death pathways. By 
  4 weeks, only C-LTMR and Ad/Ab-LTMR subtypes show any 
  overrepresentation of cell death pathways (in the populations 
  studied). Both injury-specific and apoptotic signatures in non- 
  peptidergic neurons were no longer significantly enriched, 
  consistent with a loss of axotomized nonpeptidergic afferents 
  by this late timepoint postinjury. These data suggest 
  that 
  apoptotic pathways are upregulated acutely after injury in a cell- 
  type-specific manner. 