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Temporomandibular joint inflammation decreases the voltage‐gated K + channel subtype 1.4‐immunoreactivity of trigeminal ganglion neurons in rats
Author(s) -
Takeda Mamoru,
Tanimoto Takeshi,
Nasu Masanori,
Matsumoto Shigeji
Publication year - 2008
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1016/j.ejpain.2007.04.005
Subject(s) - trigeminal ganglion , temporomandibular joint , inflammation , ganglion , chemistry , medicine , anatomy , neuroscience , pathology , biology , sensory system
Voltage‐gated K + (Kv) channels are one of the important physiological regulators of the membrane potentials in excitable cells, including sensory ganglion neurons. The aim of the present study was to investigate whether temporomandibular joint (TMJ) inflammation alters expression of Kv channel subtype 1.4 (Kv1.4) of trigeminal ganglion (TRG) neurons innervating TMJ relating allodynia (pain caused by normally innoxious stimulation), by using both behavioral and immunohistochemical techniques. TMJ inflammation was induced by injection of Complete Freund's Adjuvant (CFA) into the rat TMJ. The threshold for escape from mechanical stimulation applied to the orofacial area in TMJ inflamed rats was significantly lower than that in naïve rats. TMJ afferents were identified by fluorogold (FG) labeling. The mean numbers of Kv1.4‐/neurofilament (NF) 200(myelinated fiber marker) positive‐ and negative‐immunoreactivities FG‐labeled small‐/medium‐diameter TRG neurons in inflamed rats were significantly decreased when compared with those in the naïve rats. These findings suggest that TMJ inflammation reduces the expression of Kv1.4 subunits in the small‐/medium sized (Aδ‐/C‐) TRG neurons and this may contribute to trigeminal inflammatory allodynia in TMJ disorder. These results lead us to suggest that Kv channel openers may be a potential therapeutic agents for prevention of mechanical allodynia.