We have investigated a possible role for
vanilloid receptor 1 (TRPV1), a transducer of noxious stimuli, in the development of
neuropathic pain following injury to a peripheral branch of the trigeminal nerve. In nine adult ferrets the left lingual nerve was sectioned and recovery permitted for 3 days, 3 weeks or 3 months (3 ferrets per group). A retrograde tracer,
fluorogold, was injected into the damaged nerve to identify associated cell bodies in the trigeminal ganglion. Three further ferrets, receiving only tracer injection, served as uninjured controls. Indirect immunofluorescence for TRPV1 and image analysis was used to quantify the percentage area of staining (PAS) of TRPV1 in the left and right lingual nerves. Additionally, the proportion of
fluorogold positive and
fluorogold negative cells expressing TRPV1 in the
ganglion was determined. TRPV1 expression increased significantly at the injury site of damaged nerves 3 days after injury and this was matched by a reduction in the proportion of
fluorogold positive cells expressing TRPV1 in the
ganglion. At 3 weeks TRPV1 expression at the injury site was still high, while in the
ganglion was significantly greater than in the controls. In the 3-month recovery group TRPV1 expression in both nerve fibres and
ganglion cells, was not significantly different from controls and there were no changes in expression in the
fluorogold negative cells in the
ganglion at any time point studied. These data suggest that after injury there is an increase in the axonal transport of TRPV1 from the cell bodies to the damaged axons and this is followed by an increase in synthesis in the
ganglion. These changes in expression may be involved in development of sensory disturbances or dysaesthesia after injury.