Neuropeptide expression following ligation of the ferret lingual nerve

Changes in vanilloid receptor 1 (TRPV1) expression following lingual nerve injury

“…The recovery periods selected were the same as used in previous studies in our laboratory so that data could be compared with previous results on levels of neuropeptide expression and ectopic neural discharge after lingual nerve injury (Bird et al, 2003;Yates et al, 2000). Furthermore, changes were determined in cells associated with the damaged axons and in other cells linked to adjacent uninjured neurons.…”

“…This includes spontaneous and mechanically induced discharge from axons at the site of nerve injury (Yates et al, 2000). Although the aetiology of this ectopic activity is unclear, there is evidence to suggest that it arises from membrane instability and the abnormal accumulation of ion channels, receptors and neuropeptides (Devor, 1994;Waxman, 1999;Waxman et al, 1999Waxman et al, , 2000Bird et al, 2003). Changes also occur in the cell bodies associated with the damaged axons, in the trigeminal ganglion (Tal and Devor, 1992;Tsuboi et al, 2004).…”

The effect of a monoclonal antibody to calcitonin-gene related peptide (CGRP) on injury-induced ectopic discharge following lingual nerve injury

“…We showed that 3 days after sectioning the nerve in anaesthetised adult ferrets, up to 36% of the axons became spontaneously active and up to 35% were sensitive to mechanical stimulation [15]. In parallel immunocytochemical studies, we found an accumulation of neuropeptides at the injury site, and the maximum accumulation of peptides coincided with the periods of greatest spontaneous activity [2]. One of the neuropeptides present was calcitonin gene-related peptide (CGRP) and, in view of its known role in neural transmission and neuromodulation [13], we hypothesised that it might modify the abnormal discharge after nerve injury.…”

Evidence for anti-inflammatory and putative analgesic effects of a monoclonal antibody to calcitonin gene-related peptide

“…There is also evidence from this and other laboratories, that CGRP plays a role in trigeminal neuropathic and inflammatory pain (Loescher et al, 2001;Rodd and Boissonade, 2002;Bird et al, 2003). Within the tooth pulp CGRP is known to cause vasodilation and subsequent increased blood flow following electrical stimulation (Heyeraas et al, 1994).…”

“…The data from the present study suggest that inhibition of CGRP activity may also have analgesic efficacy in trigeminal inflammatory pain and may indicate a role for CGRP antagonism in the treatment of this type of pain. There is also evidence that CGRP may contribute to the development of ectopic activity and neuropathic pain symptoms in the trigeminal system (Loescher et al, 2001;Bird et al, 2003). However, recent work from this laboratory demonstrates that the inhibition of CGRP does not affect the level of ectopic activity at sites of nerve injury (Bowler et al, 2011).…”