Abstract
Background/aims
Tail docking neonatal piglets remains a controversial animal welfare issue. Although banned in the UK, it is widely practiced in many countries as a safeguard against tail biting among pigs reared in intensive systems. Concerns exist whether tail docking can induce chronic pain in later life. This preliminary study examined the effects of partial tail amputation on activating transcription factor 3 (ATF3), a marker of peripheral nerve injury and regeneration and NMDA-glutamate receptor NR2B subunit which participates in the mediation of chronic pain.
Methods
Procedures were performed according to the ethical guidelines for the study of experimental pain in animals. Six piglets (2–3 days old) were tail-docked (a portion of the tail amputated with sterile surgical cutters), six piglets (2–3 days old) were sham-docked. Three animals from each treatment were euthanised 7 and 56 days post-amputation. Coccygeal dorsal root ganglia (DRG) and spinal cord were collected post-mortem for immunohistochemistry.
Results
ATF3 immunoreactivity (IR) was significantly increased (p <0.05) in the DRG neurons from tail-docked piglets 7 days after tail amputation, compared with sham-docked piglets. ATF3-IR was not different in sham and tail-docked piglets 56 days post amputation. NR2B-IR was significantly increased (p < 0.05) in dorsal horn neurons in tail-docked piglets compared with intact piglets 7 days after docking. There was no difference in NR2B-IR in neurons 56 days post amputation, compared with intact piglets.
Conclusions
Increased ATF3 and NR2B-IR 7 days after tail-docking suggests that injury to the peripheral nerves in the tail was sufficient to trigger neuronal regeneration and altered dorsal horn signaling respectively, however the effects of tail-docking on neuronal regeneration and nociceptive signaling were relatively short lasting. Tail-docking neonatal piglets does not cause sustained changes in ATF3, which might suggest ongoing nerve fibre damage and NR2B which might be implicated in chronic pain.
© 2012 Scandinavian Association for the Study of Pain
