Mechanisms involved in modulation of trigeminal primary afferent activity in rats with peripheral mononeuropathy

In order to clarify the mechanisms underlying the changes in primary afferent neurons in trigeminal neuropathic pain, a chronic constriction nerve injury model of the infraorbital nerve (ION-CCI) was developed in rats. Mechanical allodynia was observed at 3 days after ION-CCI and lasted more than 14 days. Single-unit activities were recorded from the ION of anesthetized rats. C-, A beta- and A delta-units were identified on the basis of their conduction velocity. A delta-units were frequently encountered at a later period after ION-CCI. The highest A delta-spontaneous activity was recorded at 3 days after ION-CCI and progressively decreased after that, but spontaneous activity was still higher at 14 days after ION-CCI than that of naive rats. Mechanical-evoked responses of A delta-units were also highest at 3 days after ION-CCI and then gradually decreased. In consideration of these data, patch-clamp recordings were performed on medium to large size neurons of the dissociated trigeminal ganglion (TRG). Patch-clamp recordings revealed that the I-K (sustained) and I-A (transient) in rats with ION-CCI were significantly smaller than those of naive rats, and correlated with an increase in duration of repolarization phase and a decrease in duration of depolarization phase, respectively. The hyperpolarization-activated current (I-h) was significantly larger in TRG neurons of rats with ION-CCI as compared with those of naive rats. The present results suggest that I-h, I-K and I-A in A delta-afferent neurons in TRG are significantly involved in the changes in afferent spontaneous activity and mechanically evoked activity that accompany mechanical allodynia produced by trigeminal nerve injury.