Medullary dorsal horn neuronal activity in rats with persistent temporomandibular joint and perioral inflammation
Medullary dorsal horn neuronal activity in rats with persistent temporomandibular joint and perioral inflammation
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DOI：
10.1152/jn.1999.82.3.1244
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发表时间：
1999-09-01
影响因子：
2.5
通讯作者：
Ren, K
中科院分区：
文献类型：
--
作者：
Iwata, K;Tashiro, A;Ren, K
脊髓水平的研究表明，外周组织或神经损伤诱导脊髓背角神经元的过度兴奋状态，参与持续性疼痛和痛觉过敏的发展。尚未证实口面部区域的持续性损伤会导致三叉神经系统中类似的中枢过度兴奋状态。本研究的目的是进行参数分析的伤害性和非伤害性神经元的反应特性在三叉神经核尾侧（延髓背侧缘，MDH）在大鼠模型的持续性口面炎症。神经元细胞外记录和分类为低阈值机械感受性（LTM，n = 49），宽动态范围（WDR，n = 82），和伤害感受性特异性（NS，n = II）神经元根据其响应特性施加到他们的皮肤感受野（RF）的机械刺激。在记录前24 h，通过将完全弗氏佐剂（CFA）注射到颞下颌关节（TMJ）囊或口周（PO）皮肤中诱导炎症。颞下颌关节（8.66 +/- 0.61 cm（2），n = 25）和颞下颌关节（5.61 +/- 2.07 cm（2），n = 25）炎症大鼠的WDR神经元的高阈值RF的平均面积显著大于未感染大鼠（1.10 +/- 0.16 cm（2），n = 32）。颞下颌关节炎大鼠RF的平均大小也明显大于颞下颌关节炎大鼠（P < 0.01）。此外，TMJ炎症大鼠NS神经元RF的平均面积（3.74 +/- 1.44 cm（2），n = 5）显著大于未炎症大鼠NS神经元RF的平均面积（0.4 +/- 0.09 cm（2），n = 3）（P < 0.05）。背景活动在颞下颌关节和PO发炎的大鼠普遍更大的WDR和NS神经元，但在LTM神经元，与幼稚大鼠相比。颞下颌关节炎大鼠WDR神经元对伤害性机械刺激的反应性显著高于正常大鼠（P < 0.05）。WDR神经元对机械刺激的反应也在PO炎症大鼠中增加，但程度低于TMJ炎症大鼠。将CFA注射到TMJ或PO皮肤中导致LTM神经元对机械刺激的反应降低。MDH伤害性神经元对48-55 ℃加热的反应在发炎大鼠中比在未处理大鼠中更大。记录颞下颌关节（n = 4的10）或PO（n = 3的13）注射大鼠的WDR神经元的亚群响应冷却除了加热的RF，但没有等级的刺激强度的变化，他们的反应。这些结果表明，持续性口面炎症产生的MDH伤害性神经元的过度兴奋。颞下颌关节炎症导致更强大的变化，MDH伤害性神经元相比，PO炎症，与以前的研究增加炎症，增加MDH Fos蛋白表达，并增加MDH前强啡肽原mRNA表达在这个深组织orofacial疼痛和痛觉过敏模型。炎症诱导的MDH过度兴奋可能有助于与口面部深层组织疼痛状况相关的持续性疼痛的机制。
Studies at spinal levels indicate that peripheral tissue or nerve injury induces a state of hyperexcitability of spinal dorsal horn neurons that participates in the development of persistent pain and hyperalgesia. It has not been demonstrated that persistent injury in the orofacial region leads to a similar state of central hyperexcitability in the trigeminal system. The purpose of the present study was to conduct a parametric analysis of the response properties of nociceptive and nonnociceptive neurons in trigeminal nucleus caudalis (medullary dorsal hem, MDH) in a rat model of persistent orofacial inflammation. Neurons were recorded extracellularly and classified as low-threshold mechanoreceptive (LTM, n = 49), wide dynamic range (WDR, n = 82), and nociceptive-specific (NS, n = II) neurons according to their response properties to mechanical stimuli applied to their cutaneous receptive fields (RFs). The inflammation was induced 24 h before the recordings by injecting complete Freund's adjuvant (CFA) into the temporomandibular joint (TMJ) capsule or the perioral (PO) skin. The mean areas of the high-threshold RFs of WDR neurons in TMJ (8.66 +/- 0.61 cm(2), n = 25) and PO (5.61 +/- 2.07 cm(2), n = 25) inflamed rats were significantly larger than those in naive rats (1.10 +/- 0.16 cm(2), n = 32). The mean RF size in TMJ-inflamed rats also was significantly larger than that in PO-inflamed rats (P < 0.01). Furthermore the mean area of the RFs of NS neurons (3.74 +/- 1.44 cm(2), n = 5) was significantly larger in TMJ inflamed rats as compared with naive rats (0.4 +/- 0.09 cm(2), n = 3) (P < 0.05). The background activity in the TMJ- and PO-inflamed rats was generally greater in WDR and NS neurons, but less in LTM neurons, when compared with naive rats. The responses of WDR neurons to noxious mechanical stimuli were increased significantly in TMJ-inflamed rats (P < 0.05) as compared with naive rats. WDR neuronal responses to mechanical stimulation also were increased in PO-inflamed rats but to a lesser extent than in TMJ-inflamed rats. The injection of CFA into the TMJ or PO skin resulted in reduced responses of LTM neurons to mechanical stimuli. The responses of MDH nociceptive neurons to 48-55 degrees C heating were greater in inflamed rats as compared with naive rats. A subpopulation of WDR neurons recorded from TMJ (n = 4 of 10) or PO (n = 3 of 13)-injected rats responded to cooling in addition to heating of the RFs but did not grade their responses with changes in stimulus intensity. These results indicate that persistent orofacial inflammation produced hyperexcitability of MDH nociceptive neurons. TMJ inflammation resulted in more robust changes in MDH nociceptive neurons as compared with PO inflammation, consistent with previous studies of increased inflammation, increased MDH Fos-protein expression, and increased MDH preprodynorphin mRNA expression in this deep tissue orofacial model of pain and hyperalgesia. The inflammation-induced MDH hyperexcitability may contribute to mechanisms of persistent pain associated with orofacial deep tissue painful conditions.