Abstract
The aim of the present study was to investigate whether under in-vivo condition, temporomandibular joint (TMJ) inflammation alters the excitability of Aβ-trigeminal root ganglion (TRG) neuronal activity innervating the facial skin by using extracellular recording with multibarrel-electrodes. CFA was injected into the rat TMJ. A total of 36 Aβ-TRG neurons responding to electrical stimulation of the whisker pad was recorded in pentobarbital-anesthetized rats. The number of Aβ-TRG neurons with spontaneous firings and their firing rate in TMJ inflamed rats were significantly larger than those in control rats. The firing rates of their spontaneous activity in the Aβ-TRG neurons were current-dependently decreased by local iontophoretic application of a NK1 receptor antagonist (L-703,606) in inflamed, but not non-inflamed rats. The spontaneous activities were increased by iontophoretic application of substance P in both group of rats.The mechanical stimulation threshold of Aβ-TRG neurons in inflamed rats was significantly lower than that in control rats. There were no significant differences on the mechanical stimulation threshold between control and inflamed rats after iontophoretic application of L-703,606. These results suggest that TMJ inflammation can modulate the excitability of Aβ-TRG neurons innervating the facial skin via paracrine mechanism due to SP released from TRG neuronal cell body. [J Physiol Sci. 2006;56 Suppl:S178]
