title: Reversal of peripheral nerve injury-induced hypersensitivity in the postpartum period: role of spinal oxytocin.
abstract: BACKGROUND
  Physical injury, including surgery, can result in chronic pain; yet chronic pain following childbirth, including cesarean delivery in women, is rare. The mechanisms involved in this protection by pregnancy or delivery have not been explored.
  
  
  METHODS
  We examined the effect of pregnancy and delivery on hypersensitivity to mechanical stimuli of the rat hindpaw induced by peripheral nerve injury (spinal nerve ligation) and after intrathecal oxytocin, atosiban, and naloxone. Additionally, oxytocin concentration in lumbar spinal cerebrospinal fluid was determined.
  
  
  RESULTS
  Spinal nerve ligation performed at mid-pregnancy resulted in similar hypersensitivity to nonpregnant controls, but hypersensitivity partially resolved beginning after delivery. Removal of pups after delivery prevented this partial resolution. Cerebrospinal fluid concentrations of oxytocin were greater in normal postpartum rats prior to weaning. To examine the effect of injury at the time of delivery rather than during pregnancy, spinal nerve ligation was performed within 24 h of delivery. This resulted in acute hypersensitivity that partially resolved over the next 2-3 weeks. Weaning of pups resulted only in a temporary return of hypersensitivity. Intrathecal oxytocin effectively reversed the hypersensitivity following separation of the pups. Postpartum resolution of hypersensitivity was transiently abolished by intrathecal injection of the oxytocin receptor antagonist, atosiban.
  
  
  CONCLUSIONS
  These results suggest that the postpartum period rather than pregnancy protects against chronic hypersensitivity from peripheral nerve injury and that this protection may reflect sustained oxytocin signaling in the central nervous system during this period.
authors.affiliation: Wake Forest School of Medicine, Winston Salem, NC 27157, USA.
authors.forename: Silvia
authors.initials: S
authors.lastname: Gutierrez
authors.forename: Baogang
authors.initials: B
authors.lastname: Liu
authors.forename: Ken-ichiro
authors.initials: K
authors.lastname: Hayashida
authors.forename: Timothy T
authors.initials: TT
authors.lastname: Houle
authors.forename: James C
authors.initials: JC
authors.lastname: Eisenach
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D004195:Disease Models, Animal; D005260:Female; D006727:Hormone Antagonists / Q000008:administration & dosage; D006967:Hypersensitivity / Q000134:cerebrospinal fluid / Q000209:etiology* / Q000517:prevention & control*; D007278:Injections, Spinal; D009270:Naloxone / Q000008:administration & dosage; D009292:Narcotic Antagonists / Q000008:administration & dosage; D010120:Oxytocics / Q000134:cerebrospinal fluid / Q000494:pharmacology*; D010121:Oxytocin / Q000134:cerebrospinal fluid / Q000494:pharmacology*; D059348:Peripheral Nerve Injuries / Q000134:cerebrospinal fluid / Q000150:complications*; D010812:Physical Stimulation; D049590:Postpartum Period; D051381:Rats; D017207:Rats, Sprague-Dawley; D013127:Spinal Nerves / Q000187:drug effects; D014668:Vasotocin / Q000008:administration & dosage / Q000031:analogs & derivatives; D014886:Weaning
chemical_list: D006727:Hormone Antagonists; D009292:Narcotic Antagonists; D010120:Oxytocics; C047046:atosiban; D009270:Naloxone; D010121:Oxytocin; D014668:Vasotocin