抄録
The neuronal mechanism underlying trigeminal neuropathic pain was studied in the rats with inferior alveolar nerve (IAN) transection. There is evidence that activated glia contribute to trigeminal neuropathic pain following peripheral nerve injury. However, the underlying mechanism of grial involvement in nerve injury induced neuropathic pain in the trigeminal region is not known. We studied the involvement of astrocytes in neuropathic pain in rats with IAN transection. IAN transection (IAN group) or sham operation (Sham group) was performed in SD rats under adequate anesthesia (50mg/kg, i.p.). Single unit recordings from the trigeminal spinal nucleus caudalis (Vc) were done in IAN or Sham group. Topical administration of fluoroacetate (FA, 1 mM) to the Vc attenuated noxious mechanical and heat responses in IAN group (P<0.05), but not in Sham group. The neuronal responses recovered after local application of glutamine in FA-treated rats. The pERK expression after IAN transection following noxious mechanical stimulation was depressed after the intrathecal (i.t.) administration of FA to Vc (P<0.05). The i.t. application of FA also produced a prolongation of the face withdrawal latency (p<0.01).The present findings suggest that the glutamine-glutamate shuttle in the astroglia is involved in the hyperexcitability of Vc nociceptive neurons, resulting in the trigeminal neuropathic pain following trigeminal nerve injury. [J Physiol Sci. 2008;58 Suppl:S151]
