Departments of Complete Denture Prosthodontics and.
Physiology, Nihon University School of Dentistry, Tokyo, Japan.
Pain. 2019 Jun;160(6):1342-1360. doi: 10.1097/j.pain.0000000000001521.
Trigeminal spinal subnucleus caudalis (Vc) neurons that project to the ventral posteromedial thalamic nucleus (VPM) and parabrachial nucleus (PBN) are critical for orofacial pain processing. We hypothesized that persistent trigeminal nerve injury differentially alters the proportion of Vc neurons that project to VPM and PBN in a modality-specific manner. Neuroanatomical approaches were used to quantify the number of Vc neurons projecting to VPM or PBN after chronic constriction injury of the infraorbital nerve (ION-CCI) and subsequent upper-lip stimulation. Male rats received injections of retrograde tracer fluorogold into the contralateral VPM or PBN on day 7 after ION-CCI, and at 3 days after that, either capsaicin injection or noxious mechanical stimulation was applied to the upper lip ipsilateral to nerve injury. Infraorbital nerve chronic constriction injury rats displayed greater forelimb wiping to capsaicin injection and mechanical allodynia of the lip than sham rats. Total cell counts for phosphorylated extracellular signal-regulated kinase-immunoreactive (pERK-IR) neurons after capsaicin or mechanical lip stimuli were higher in ION-CCI than sham rats as was the percentage of pERK-IR PBN projection neurons. However, the percentage of pERK-IR VPM projection neurons was also greater in ION-CCI than sham rats after capsaicin but not mechanical lip stimuli. The present findings suggest that persistent trigeminal nerve injury increases the number of Vc neurons activated by capsaicin or mechanical lip stimuli. By contrast, trigeminal nerve injury modifies the proportion of Vc nociceptive neurons projecting to VPM and PBN in a stimulus modality-specific manner and may reflect differential involvement of ascending pain pathways receiving C fiber and mechanosensitive afferents.
三叉神经脊束核尾侧亚核（Vc）神经元投射到腹后内侧丘脑核（VPM）和臂旁核（PBN）对于口腔面部疼痛处理至关重要。我们假设，持续性三叉神经损伤以一种模态特异性的方式改变了投射到 VPM 和 PBN 的 Vc 神经元的比例。神经解剖学方法用于定量分析眶下神经慢性缩窄性损伤（ION-CCI）后和随后的上唇刺激后，投射到 VPM 或 PBN 的 Vc 神经元的数量。雄性大鼠在 ION-CCI 后第 7 天将逆行示踪剂荧光金注入对侧 VPM 或 PBN，并在那之后的第 3 天，对同侧神经损伤的上唇进行辣椒素注射或有害机械刺激。眶下神经慢性缩窄性损伤大鼠对辣椒素注射的前肢擦拭和唇部机械性痛觉过敏的反应比假手术大鼠更为明显。与假手术大鼠相比，ION-CCI 大鼠在辣椒素或机械性唇刺激后，磷酸化细胞外信号调节激酶免疫反应性（pERK-IR）神经元的总细胞计数更高，PBN 投射神经元中 pERK-IR 的比例也更高。然而，与机械性唇刺激相比，ION-CCI 大鼠在辣椒素刺激后，pERK-IR 的 VPM 投射神经元的比例也更高。本研究结果表明，持续性三叉神经损伤增加了对辣椒素或机械性唇刺激有反应的 Vc 神经元的数量。相比之下，三叉神经损伤以一种刺激模态特异性的方式改变了投射到 VPM 和 PBN 的 Vc 伤害性神经元的比例，这可能反映了接受 C 纤维和机械敏感传入的上行疼痛通路的不同参与。
