Temporomandibular joint inflammation potentiates the excitability of trigeminal root ganglion neurons innervating the facial skin in rats
Temporomandibular joint inflammation potentiates the excitability of trigeminal root ganglion neurons innervating the facial skin in rats
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DOI：
10.1152/jn.00631.2004
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发表时间：
2005-05-01
影响因子：
2.5
通讯作者：
Matsumoto, S
中科院分区：
文献类型：
--
作者：
Takeda, M;Tanimoto, T;Matsumoto, S
本研究的目的是测试的假设，颞下颌关节（TMJ）炎症改变三叉神经根神经节（TRG）神经元支配面部皮肤的兴奋性，通过使用行为，电生理，分子和免疫组化方法。将完全弗氏佐剂（CFA）注射到大鼠TMJ中以产生炎症。颞下颌关节炎大鼠逃避机械刺激的阈值明显低于未受刺激的大鼠。用2%荧光金（FG）标记支配炎症颞下颌关节的TRG神经元。与正常大鼠相比，炎症大鼠P物质（SP）免疫反应阳性神经元的数量显著增加。另一方面，中，大直径TRG神经元（> 30 μ m）支配面部皮肤标记FG注射到面部皮肤。在FG标记的皮肤TRG神经元中，SP（100 nM）诱导的膜去极化在炎症大鼠中的发生率（中：73.3%，大：85.7%）大于在幼稚大鼠中的发生率（中：29.4%，大：0%）。此外，SP应用显着增加放电率引起的去极化脉冲在炎症大鼠的神经元与那些幼稚大鼠相比。定量单细胞RT-PCR分析显示，在FG标记的TRG神经元在炎症大鼠的NK 1受体mRNA的表达增加相比，在幼稚大鼠。SP和NK 1受体/神经丝200阳性免疫反应TRG神经元支配的面部皮肤（FG标记）在发炎大鼠的数量显着增加，与那些在幼稚大鼠。这些结果表明，颞下颌关节炎症可以改变中，大直径的TRG神经元支配的面部皮肤的兴奋性和SP/NK 1受体在其索马的增加可能有助于三叉神经炎性异常性疼痛的颞下颌关节紊乱的机制。
The aim of this study was to test the hypothesis that temporomandibular joint (TMJ) inflammation alters the excitability of trigeminal root ganglion (TRG) neurons innervating the facial skin, by using behavioral, electrophysiological, molecular, and immunohistochemical approaches. Complete Freund's adjuvant (CFA) was injected into the rat TMJ to produce inflammation. The threshold for escape from mechanical stimulation applied to the orofacial area in TMJ-inflamed rats was significantly lower than that in naive rats. The TRG neurons innervating the inflamed TMJ were labeled by 2% Fluorogold (FG) injection into the TMJ. The number of FG-labeled substance P (SP)-immunoreactive neurons in the inflamed rats was significantly increased compared with that in the naive rats. On the other hand, medium- and large-diameter TRG neurons ( > 30 mu m) innervating the facial skin were labeled by FG injection into the facial skin. In the FG-labeled cutaneous TRG neurons, the occurrence of SP ( 100 nM) induced membrane depolarization in inflamed rats ( medium: 73.3%, large : 85.7%) was larger than that in the naive rats ( medium: 29.4%, large : 0%). In addition, SP application significantly increased the firing rate evoked by depolarizing pulses in the neurons of inflamed rats compared with those of naive rats. Quantitative single-cell RTPCR analysis showed the increased expression of mRNA for the NK1 receptor in FG-labeled TRG neurons in inflamed rats compared with that in naive rats. The numbers of SP and NK1 receptors/neurofilament 200 positive immunoreactive TRG neurons innervating the facial skin (FG-labeled) in the inflamed rats were significantly increased compared with those seen in naive rats. These results suggest that TMJ inflammation can alter the excitability of medium- and large-diameter TRG neurons innervating the facial skin and that an increase in SP/NK1 receptors in their soma may contribute to the mechanism underlying the trigeminal inflammatory allodynia in the TMJ disorder.