(Background and Goal of study) The trigeminal nerve may be damaged during maxillofacial injury or surgical procedures. Traumatic trigeminal neuropathy is particularly resistant to standard pharmacological treatment. Substantial evidences revealed that nicotinic acetylcholine receptors (nAChRs) are widely expressed in the spinal cord and modulate nociceptive transmission. Spinal administration of the nicotinic agonists has been shown to produce antinociception. The contribution of spinal nAChRs in inhibiting the trigeminal neuropathic pain remained unclear. Chronic constriction injury to the infraorbital nerve (ION-CCI) has proven a useful model for trigeminal neuropathic pain. The present study evaluated the possible role of spinal nAChRs in ION-CCI rat model. 
(Material and Methods) Male Sprague Dawley rats underwent unilateral CCI to the right ION. Two nylon (5-0) ligatures were tied around the ION. Series of von Frey filaments were used to determine pain hypersensitivity to mechanical stimulation on day 14 after surgery. A polyethylene (PE-10) catheter was implanted for upper cervical spinal injection of drugs. The rats were allowed to recover for 7 days. The potential anti-allodynic effects from intrathecal administration of a nAChR agonist nicotine and an alpha 7 nAChR agonist PNU 282987 were examined. In addition, the role of nAChR and alpha 7 nAChR in these effects was assessed by determine whether the anti-allodynic effects were prevented by intrathecal administration of a nAChR antagonist mecamylamine or an alpha 7 nAChR antagonist methyllycaconitine. The time course data for the dose-response effects were analyzed by two-way analysis of variance and Tukey-Kramer multiple-comparison test.
(Results and Discussion) Intrathecal administration of nicotine and PNU 282987 increased mechanical thresholds in a dose dependent manner (P <0.05). Mecamylamine significantly reduced the anti-allodynic effect of nicotine. Methyllycaconitine significantly reduced the anti-allodynic effect of PNU 282987.
(Conclusions) The results indicated that spinal nAChRs and alpha 7 nAChRs may play an important role in a rat model of trigeminal neuropathic pain.

Intratecal administration of nicotinic agonists attenuates pain-related behavior in a rat model of trigeminal neuropathic pain