A study on the role of neurotrophines in trigeminal neuropathy and sensory abnormality

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A chronic compression injury to the trigeminal ganglion by an injection of medical silicone via the foramen ovale was induced on seven anesthetized rats (TNP group). The same dissection to the TNP group without injecting silicone was performed on another seven rats (SHM group). Seven rats received cysternal injection of NGF (NGF group) and another seven rats received BDNF (BDNF group). The TNP group and the NGF group showed heat hyperalgesia from fourth post-operative day and mechanical allodynia from seventh post-operative day. However, the SHM and the BDNF groups did not show any significant decrease of thresholds during the time course. These results showed that NGF induces central sensitization by itself and BDNF doesn't have such an effect. In the next study, rats received 200 mg/kg/day or 2000 mg/kg/day of i.p. GSH (NGF-200 group : n-7 and NGF-2000 group : n=7) and 4 mg/kg/day of DEM instead of GSH (NGF-DEM group : n=7) from three days before the NGF injection. Control groups to these groups were prepared by performing sham treatment instead of the NGF injection (SHM-2000 and SHM-DEM groups). NGF-200 and NGF-DEM groups showed decrease of head withdrawal latency from radiant heat stimulation from fourth and seventh post-operative days, respectively. In contrast, NGF-2000, SHM-2000 and SHM-DEM groups did not show any significant behaviors suggesting heat- and mechano-hyperalgesia or allodynia. These results revealed that GSH prevented hyperalgesia by suppressing hypersensitization of the trigeminal nucleus cells that is induced by NGF.