text: Earlier studies postulated that a lack of neurotrophic support 
  underlies neuronal loss, which is supported by the observation 
  that exogenous GDNF treatment at the time of injury, or shortly 
  after, 
  terminals 
  posttransection.5 We sought to use the DRG neurons from 
  MrgDCreERT2;Ai32 mice to test this postulate and establish an 
  in vitro platform capable of probing the molecular basis of loss, 
  with axonal transection during isolation providing a correlate 
  for in vivo nerve injury (Figs. 5A–E). Twenty-four hours after 
  plating, YFP was expressed by 16.3 6 1.3% of DRG neurons, 
  which was reduced to 11.8 6 1.7% after 28 days of culture in 
  the presence of exogenous GFs, NGF and GDNF (Fig. 5F). 
  in the absence of GFs, YFP1 neurons only 
  However, 
  accounted for 1.7 6 0.6% of neurons after 28 days, 
  accompanied by an apparent reduction in the overall number 
  of neurons within the culture, despite all conditions being 
  seeded at the same initial density (Figs. 5C and F). YFP1 cell 
  loss was partially rescued by the presence of GDNF, but not 
  NGF alone, in the culture media (Figs. 5D–F). These results 
  contrasted with experiments using neurons derived from 
  CalcaCreERT2;Ai32 mice, in which we observed no change in 
  the proportion of neurons that were Calca-YFP1 after 28 days 
  in culture, regardless of exogenous GF addition (Figs. 5G–L). 
  Collectively, these data support the use of DRG cultures to 
  probe the mechanisms underlying selective loss of sensory 
  neurons following nerve injury and suggest a role for trophic 
  support, particularly by GDNF signaling, in preventing the loss 
  of nonpeptidergic nociceptors. 
  
  rescues the loss of  IB4-binding central 