text: While definitively characterizing loss of molecularly defined 
  subpopulations was challenging before the advent of recombi- 
  nase driver lines, a consensus emerged that small-diameter 
  neurons are more vulnerable to nerve injury–induced loss.50,53 
  Our data support this consensus and extend it to reveal that while 
  there is a generalized partial loss of C-fiber populations including 
  CGRP- and Trpm8-expressing neurons, Mrgprd-expressing 
  neurons are particularly sensitive to loss. This selective vulnera- 
  bility has been hinted at previously by the stark reduction in the 
  number of DRG neurons and their central terminals that bind IB4 
  and express canonical markers such as the P2X3 receptor 
  following nerve injury.5,8,29,36 Type 1a glomeruli are also reduced 
  in lamina II, suggesting a structural loss of central terminals and 
  not simply a loss of IB4-binding.2 However, it was not clear 
  whether these data represented phenotypic changes in non- 
  peptidergic nociceptors or frank loss of neurons. We describe 
  neuron loss that is delayed (occurring .7 days postinjury) with 
  respect to histochemical and structural changes (occurring 1- 
  5 days postinjury2,29), suggesting that these changes precede 
  and are not in themselves indicative of neuron loss. 