Trigeminal-rostral ventromedial medulla circuitry is involved in orofacial hyperalgesia contralateral to tissue injury.
Trigeminal-rostral ventromedial medulla circuitry is involved in orofacial hyperalgesia contralateral to tissue injury.
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DOI：
10.1186/1744-8069-8-78
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发表时间：
2012-10-23
期刊：
影响因子：
3.3
通讯作者：
Ren K
中科院分区：
文献类型：
--
作者：
Chai B;Guo W;Wei F;Dubner R;Ren K
我们的前期研究表明，完全弗氏佐剂（CFA）诱导的咬肌炎症和三叉神经脊束核（Vi/Vc）极间亚核/尾侧亚核过渡区（Vi/Vc）微量注射促炎细胞因子白细胞介素-1 β（IL-1β）可诱导大鼠对侧口面痛觉过敏。我们还表明，对侧的痛觉过敏会随着延髓头端腹内侧（RVM）（下行疼痛调制的关键部位）的损伤而减弱。在这里，我们研究了参与RVM-Vi/Vc电路介导对侧口面痛觉过敏后，注射CFA到咬肌。在同侧Vi/Vc区微量注射IL-1受体拮抗剂（5 nmol，n=6）可减弱CFA引起的对侧痛觉过敏，但对同侧痛觉过敏无影响。RVM内给药后注射NK 1受体拮抗剂RP 67580（0.5-11.4 nmol）和L-733，060（0.5-11.4 nmol）可减弱CFA诱导的双侧痛觉过敏和IL-1β诱导的双侧痛觉过敏。在咬肌内注射CFA之前RVM神经元中的5-羟色胺耗竭防止CFA注射后1-3天对侧痛觉过敏的发展。直接微量注射选择性5-HT_3受体拮抗剂Y-25130（2.6-12.9 nmol）抑制对侧Vi/Vc中的5-HT_3受体，减弱CFA诱导的对侧痛觉过敏。病变的同侧Vc阻止同侧痛觉过敏的发展，但不能阻止对侧痛觉过敏的发展。这些结果表明，CFA诱导的对侧口面痛觉过敏的发展介导的RVM-Vi/Vc电路的下行易化机制。
Our previous studies have shown that complete Freund’s adjuvant (CFA)-induced masseter inflammation and microinjection of the pro-inflammatory cytokine interleukin-1β (IL-1β) into the subnucleus interpolaris/subnucleus caudalis transition zone of the spinal trigeminal nucleus (Vi/Vc) can induce contralateral orofacial hyperalgesia in rat models. We have also shown that contralateral hyperalgesia is attenuated with a lesion of the rostral ventromedial medulla (RVM), a critical site of descending pain modulation. Here we investigated the involvement of the RVM-Vi/Vc circuitry in mediating contralateral orofacial hyperalgesia after an injection of CFA into the masseter muscle. Microinjection of the IL-1 receptor antagonist (5 nmol, n=6) into the ipsilateral Vi/Vc attenuated the CFA-induced contralateral hyperalgesia but not the ipsilateral hyperalgesia. Intra-RVM post-treatment injection of the NK1 receptor antagonists, RP67580 (0.5-11.4 nmol) and L-733,060 (0.5-11.4 nmol), attenuated CFA-induced bilateral hyperalgesia and IL-1β induced bilateral hyperalgesia. Serotonin depletion in RVM neurons prior to intra-masseter CFA injection prevented the development of contralateral hyperalgesia 1–3 days after CFA injection. Inhibition of 5-HT3 receptors in the contralateral Vi/Vc with direct microinjection of the select 5-HT3 receptor antagonist, Y-25130 (2.6-12.9 nmol), attenuated CFA-induced contralateral hyperalgesia. Lesions to the ipsilateral Vc prevented the development of ipsilateral hyperalgesia but did not prevent the development of contralateral hyperalgesia. These results suggest that the development of CFA-induced contralateral orofacial hyperalgesia is mediated through descending facilitatory mechanisms of the RVM-Vi/Vc circuitry.
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影响因子：
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通讯作者：
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