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526593 
Journal Article 
Temporomandibular joint inflammation decreases the voltage-gated K+ channel subtype 1.4-immuno reactivity of trigeminal ganglion neurons in rats 
Takeda, M; Tanimoto, T; Nasu, M; Matsumoto, S 
2008 
Yes 
European Journal of Pain
ISSN: 1090-3801 
WILEY 
HOBOKEN 
12 
2 
189-195 
English 
17584507 
WOS:000252676500007 
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 naive rats. TMJ afferents were identified by fluorogold (FG) labeling. The mean numbers of Kv 1.4-/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 naive rats. These findings suggest that TMJ inflammation reduces the expression of Kv1.4 subunits in the small-/medium sized (A delta/C-) TRG neurons and this may contribute to trigeminal inflammatory allodynia in TMJ disorder. These results lead LIS to Suggest that Kv channel openers may be a potential therapeutic agents for prevention of mechanical allodynia. (c) 2007 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights reserved. 
inflammation; trigeminal ganglion neurons; Kv1.4; immunohistochemistry; allodynia; alpha-gene expression; dorsal-root ganglia; mechanical allodynia; potassium channels; down-regulation; substance-p; pain; currents; capsaicin; receptor