text: Neuronal 
  loss has been proposed as a key contributor to poor 
  functional recovery following nerve injury,54 and biased survival of 
  types might be expected to contribute to 
  different afferent 
  modality-specific sensory deficits. Beyond loss of function, does 
  DRG neuron loss contribute to chronic pain, in either an adaptive or 
  maladaptive manner? Intrathecal delivery of GDNF is neuro- 
  protective and reverses the reduction in the number of IB4-binding 
  DRG neurons and central terminals seen following transection.5 
  Treatment is concurrently analgesic and abrogates pain-related 
  behaviors.7,60 However, the pleiotropic nature of GDNF makes it 
  impossible to directly attribute the analgesic effects to the reversal 
  of neuron loss. Indeed, it is possible that GDNF exerts its effect by 
  actions on intact nonpeptidergic nociceptive afferents,52 activation 
  of which is known to drive aversive behaviors in the neuropathic 
  state.62 These data leave the contribution of nonpeptidergic 
  nociceptor loss to behavior in the GDNF treatment paradigm 
  ambiguous. Other pharmacological approaches have been found 
  effective at reversing a neuronal 
  loss in rodent models, but the 
  impact on pain behavior was not studied.21,22 