Dopaminergic Modulation of Orofacial Mechanical Hypersensitivity Induced by Infraorbital Nerve Injury
Dopaminergic Modulation of Orofacial Mechanical Hypersensitivity Induced by Infraorbital Nerve Injury
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DOI：
10.3390/ijms21061945
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发表时间：
2020-03
影响因子：
5.6
通讯作者：
Hiroharu Maegawa;Nayuka Usami;Chiho Kudo;H. Hanamoto;H. Niwa
中科院分区：
文献类型：
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作者：
Hiroharu Maegawa;Nayuka Usami;Chiho Kudo;H. Hanamoto;H. Niwa
虽然下行多巴胺能控制系统尚未完全了解，但据报道下丘脑 A11 核是其主要来源。为了更好地了解该系统，特别是 A11 核对神经性疼痛的影响，我们创建了大鼠眶下神经慢性压迫损伤模型 (ION-CCI)。 ION-CCI 大鼠腹腔注射喹吡罗（一种多巴胺 D2 受体激动剂）。 ION-CCI 大鼠在 A11 核中显微注射喹吡罗、蝇蕈醇 [一种 γ-氨基丁酸 A 型 (GABAA) 受体激动剂] 或神经毒素 6-羟基多巴胺 (6-OHDA)。使用冯弗雷丝作为上颌胡须垫皮肤上的机械刺激；评估对刺激的行为和免疫组织化学反应。腹腔注射喹吡罗并显微注射喹吡罗或蝇蕈醇后，ION-CCI大鼠表现出缩头阈值增加，三叉神经尾亚核（Vc）浅层磷酸化细胞外信号调节激酶（pERK）免疫反应性（pERK-IR）细胞数量减少。 6-OHDA 显微注射后，ION-CCI 大鼠表现出缩头阈值降低，Vc 中 pERK-IR 细胞数量增加。我们的研究结果表明，下行多巴胺能控制系统参与三叉神经病理性疼痛的调节。
While the descending dopaminergic control system is not fully understood, it is reported that the hypothalamic A11 nucleus is its principle source. To better understand the impact of this system, particularly the A11 nucleus, on neuropathic pain, we created a chronic constriction injury model of the infraorbital nerve (ION-CCI) in rats. ION-CCI rats received intraperitoneal administrations of quinpirole (a dopamine D2 receptor agonist). ION-CCI rats received microinjections of quinpirole, muscimol [a gamma-aminobutyric acid type A (GABAA) receptor agonist], or neurotoxin 6-hydroxydopamine (6-OHDA) into the A11 nucleus. A von Frey filament was used as a mechanical stimulus on the maxillary whisker pad skin; behavioral and immunohistochemical responses to the stimulation were assessed. After intraperitoneal administration of quinpirole and microinjection of quinpirole or muscimol, ION-CCI rats showed an increase in head-withdrawal thresholds and a decrease in the number of phosphorylated extracellular signal-regulated kinase (pERK) immunoreactive (pERK-IR) cells in the superficial layers of the trigeminal spinal subnucleus caudalis (Vc). Following 6-OHDA microinjection, ION-CCI rats showed a decrease in head-withdrawal thresholds and an increase in the number of pERK-IR cells in the Vc. Our findings suggest the descending dopaminergic control system is involved in the modulation of trigeminal neuropathic pain.