IADR Abstract Archives

Changes in P2X3 Expression Following Lingual Nerve Injury

Objectives: Lingual nerve injury leads to receptor remodelling at the injury site and in injured cells in the trigeminal ganglion. These changes may contribute to the development of injury-induced pain. P2X3, an ion channel activated by ATP, is expressed in nociceptive afferents and could play a role in neuropathic pain. We have quantified changes in P2X3 expression following lingual nerve injury.

Methods: The left lingual nerve was sectioned in nine anaesthetised adult ferrets and recovery permitted for 3 days, 3 weeks or 3 months (3 ferrets per group). Three days before the end of the recovery period a retrograde tracer, fluorogold, was applied to the nerve to allow identification of injured cell bodies in the trigeminal ganglion. After perfusion fixation under anaesthesia (sodium pentobarbitone; induction 42mg/kg i.p., maintenance 3mg/kg i.v.), the lingual nerves and trigeminal ganglia were harvested and processed using indirect immunofluorescence for P2X3. Image analysis was used to quantify the percentage area of staining at the injury site. In addition, the proportion of injured cells in the trigeminal ganglion that expressed P2X3 was determined. Comparisons were made with results from control animals that only received the tracer injection.

Results: No significant change in P2X3 expression was observed in the injured nerves at any of the recovery periods, when compared to uninjured or contralateral controls. Fewer trigeminal ganglion cells expressed P2X3 3 days (9.0±1.9[SEM]%) and 3 weeks (8.2±1.3%) after injury than in control ganglia (11.7±7.4%), but this difference was not significant (p>0.05). Three months after injury, P2X3 expression in ganglion cells was similar to controls (12.2±3.2%, p>0.05).

Conclusion: These data show no significant changes in P2X3 expression following lingual nerve injury. This suggests that changes in P2X3 expression do not play a primary role in the development of lingual nerve injury-induced dysaesthesia.

Supported by the MRC (UK) and GlaxoSmithKline


Division: British and Scandinavian Divisions Meeting
Meeting: 2007 British and Scandinavian Divisions Meeting (Durham, England)
Location: Durham, England
Year: 2007
Final Presentation ID: 94
Abstract Category|Abstract Category(s): Neuroscience / TMJ
Authors
  • Biggs, James E.  ( University of Sheffield, Sheffield, N/A, United Kingdom )
  • Yates, Julian M.  ( University of Sheffield, Sheffield, N/A, United Kingdom )
  • Clayton, Nick M.  ( GlaxoSmithKline, Harlow, N/A, United Kingdom )
  • Loescher, Alison R.  ( University of Sheffield, Sheffield, N/A, United Kingdom )
  • Robinson, Peter P.  ( University of Sheffield, Sheffield, N/A, United Kingdom )
  • Boissonade, Fiona M.  ( University of Sheffield, Sheffield, N/A, United Kingdom )
  • SESSION INFORMATION
    Poster Session
    Neurosciences / TMJ
    04/03/2007