Iontophoretic application of an A-type potassium channel blocker to the trigeminal ganglion neurons enhances the excitability of Aδ- and C-neurons innervating the temporomandibular joint in rats

The present study tested the hypothesis that under in vivo conditions the iontophoretic application of a IA channel blocker, 4-aminopyridine (4-AP), to the TRG neurons changes the properties of Aδ-/C-TRG neurons that innervate the temporomandibular joint (TMJ) region, using extracellular electrophysiological recording with multi-barrel electrodes in pentobarbital-anesthetized rats. A total of twenty-one neurons (Aδ-: 76%; C-: 24%) responded to electrical stimulation of the TMJ region in pentobarbital-anesthetized rats. TMJ electrical stimulation-induced discharges of Aδ/C-neurons were significantly potentiated in current dependent manner (30–70 nA) by iontophoretic application of 4-AP into the TRGs. The spontaneous firing rates of Aδ- and C-neurons were also increased by 4-AP in a current-dependent manner (30–70 nA). The mean threshold current that evoked spontaneous discharges of C-neurons was significantly lower than that of Aδ-neurons. Moreover, the mean relative threshold current for electrical stimulation of TMJ-induced response of C-TRG neurons was significantly lower than that of Aδ-neuron. The relative firing rate of C-neurons induced by 4-AP-treatment (70 nA) was significantly higher than for Aδ-neurons. These results suggest that the application of 4-AP enhanced Aδ/C-TRG neuronal activities innervating the TMJ in vivo and C-neurons had significantly higher sensitivity for 4-AP than Aδ-neurons.

► We examined effect of 4-AP on the excitability of TRG neurons that innervate the TMJ region
► Application of 4-AP into the TRGs enhanced Aδ/C-TRG neuronal activities.
► C-neurons had significantly higher sensitivity for 4-AP than Aδ-neurons.
► IA channels in C-TRG neurons play an important role in TMJ inflammatory pain than Aδ-neurons.