Role of paracrine mechanism on the excitability of trigeminal root ganglion following temporomandibular joint disorder

旁分泌机制对颞下颌关节紊乱后三叉神经根神经节兴奋性的影响

• 批准号: 15591980
• 负责人: TAKEDA Mamoru
• 金额: $ 2.24万
• 依托单位: The Nippon Dental University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2003
• 资助国家: 日本
• 起止时间: 2003 至 2004
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-15591980/
• 关键词: trigeminal root ganglion; NK1 receptor; inflammation; paracrine; perforated-patch clamp; Iontophoresis; extracellular recording; Substance P; 顎関節炎; SubstanceP; アロデニア; パッチクランプ法

The aim of the present study to investigate whether the local release of substance P (SP) from the trigeminal root ganglion (TRG) neurons innervating temporomandibular joint (TMJ) modulates the excitability of Aβ-TRG neurons innervating the facial skin via the paracrine mechanism, in rats after TMJ inflammation. Complete Freund's adjuvant (CFA) was injected into the rat TMJ to produce inflammation. To compare the difference of SP responsiveness between naive and inflamed rats, we have conducted following experiments by using behavioral (mechanical stimulation threshold), electrophysiological (patch-clamp / extracellular recording with iontophoretic application for TRG neurons), molecular (mRNA for NK1) and immunohistochemical (functional protein for SP/NK1 receptor) approaches. The threshold for escape from mechanical stimulation applied to the orofacial area in TMJ-inflamed rats was significantly decreased. The number of SP-immunoreactive TMJ neurons in the inflamed rats was significa … More ntly increased. In cutaneous medium- and large-diameter TRG neurons (>30μm), the occurrence of SP (100nM) induced membrane depolarization in inflamed rats was larger than that in the naive rats. Quantitative single-cell reverse transcription-polymerase chain reaction analysis showed the increased expression of mRNA for NK1 receptor in cutaneous TRG neurons in inflamed rats. The numbers of SP/NK1 receptors / neurofilament 200 positive cutaneous TRG neurons in the inflamed rats were significantly increased. The mechanical stimulation threshold of Aβ-TRG neurons in inflamed rats was significantly lower than that in naive rats. There were no significant differences on the mechanical stimulation threshold between naive and inflamed rats after iontophoretic application of NK1 receptor antagonists. These results suggest that TMJ inflammation can alter the excitability of Aβ-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. Less

本研究旨在探讨颞下颌关节（TMJ）炎症后三叉神经根神经节（TRG）神经元P物质（SP）的局部释放是否通过旁分泌机制调节支配面部皮肤的Aβ-TRG神经元的兴奋性。在大鼠TMJ内注射完全弗氏佐剂（CFA）引起炎症。为了比较幼年大鼠和炎症大鼠SP反应性的差异，我们通过行为（机械刺激阈值）、电生理（膜片钳/细胞外记录与TRG神经元的离子电泳应用）、分子（NK1的mRNA）和免疫组织化学（SP/NK1受体的功能蛋白）方法进行了以下实验。颞下颌关节炎症大鼠的机械刺激逃逸阈值明显降低。炎症大鼠颞下颌关节中sp免疫反应性神经元数量明显增加。在皮肤中、大直径TRG神经元（bbb30 μm）中，炎症大鼠SP （100nM）诱导的膜去极化发生率大于未发作大鼠。定量单细胞逆转录-聚合酶链反应分析显示，炎症大鼠皮肤TRG神经元中NK1受体mRNA表达增加。炎症大鼠皮肤中SP/NK1受体/神经丝200阳性TRG神经元数量显著增加。炎症大鼠a - β- trg神经元的机械刺激阈值明显低于幼稚大鼠。未成熟大鼠和炎症大鼠在使用NK1受体拮抗剂后的机械刺激阈值无显著差异。这些结果表明，TMJ炎症可改变支配面部皮肤的Aβ-TRG神经元的兴奋性，其胞体中SP / NK1受体的增加可能参与了TMJ疾病三叉神经炎性异常性痛的机制。少

项目成果

Temporomandibukar joint inflammation potentiates the excitability of trigeminal root ganglion neurons innervating the facial skin in rats

颞下颌关节炎症增强大鼠面部皮肤三叉神经根神经元的兴奋性

• 发表时间: 2005
• 期刊: Journal of Neurophysiology (in press)
• 作者: M.Takeda et al.

Temporomandibular joint inflammation potentiates the excitability of trigeminal root ganglion neurons innervating facial skin in the rats

颞下颌关节炎症增强大鼠面部皮肤三叉神经根神经元的兴奋性

• 发表时间: 2005
• 期刊: Journal of Neurophysiology (in press)
• 作者: M.Takeda;T.Tanimoto;M.Ikeda;M.Nasu;J.Kadoi;Y.Shima;H.Ohta;S.Matsumoto.;M.Takeda et al.
• 通讯作者: M.Takeda et al.

Temporomandibular joint inflammation potentiates the excitability of trigeminal root ganglion neurons innervating the facial skin in rats

• DOI: 10.1152/jn.00631.2004
• 发表时间: 2005-05-01
• 期刊: JOURNAL OF NEUROPHYSIOLOGY
• 影响因子: 2.5
• 作者: Takeda, M;Tanimoto, T;Matsumoto, S
• 通讯作者: Matsumoto, S