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Altered activity in the nucleus raphe magnus underlies cortical hyperexcitability and facilitates trigeminal nociception in a rat model of medication overuse headache
BMC Neuroscience ( IF 2.4 ) Pub Date : 2019-10-21 , DOI: 10.1186/s12868-019-0536-2
Prangtip Potewiratnanond 1 , Supang Maneesri le Grand 2 , Anan Srikiatkhachorn 3 , Weera Supronsinchai 4
Affiliation  

BackgroundThe pathogenesis of medication overuse headache (MOH) involves hyperexcitability of cortical and trigeminal neurons. Derangement of the brainstem modulating system, especially raphe nuclei may contribute to this hyperexcitability. The present study aimed to investigate the involvement of the nucleus raphe magnus (NRM) in the development of cortical and trigeminal hyperexcitability in a rat model of MOH.ResultsChronic treatment with acetaminophen increased the frequency of cortical spreading depression (CSD) and the number of c-Fos-immunoreactive (Fos-IR) neurons in the trigeminal nucleus caudalis (TNC). In the control group, muscimol microinjected into the NRM increased significantly the frequency of CSD-evoked direct current shift and Fos-IR neurons in the TNC. This facilitating effect was not found in rats with chronic acetaminophen exposure. In a model of migraine induced by intravenous systemic infusion of nitroglycerin (NTG), rats with chronic exposure to acetaminophen exhibited significantly more frequent neuronal firing in the TNC and greater Fos-IR than those without the acetaminophen treatment. Muscimol microinjection increased neuronal firing in the TNC in control rats, but not in acetaminophen-treated rats. The number of Fos-IR cells in TNC was not changed significantly.ConclusionChronic exposure to acetaminophen alters the function of the NRM contributing to cortical hyperexcitability and facilitating trigeminal nociception.

中文翻译:

在药物过度使用性头痛的大鼠模型中,大中缝核活动的改变是皮质过度兴奋的基础,并促进三叉神经伤害感受

背景药物过度使用性头痛 (MOH) 的发病机制涉及皮质和三叉神经元的过度兴奋。脑干调节系统的紊乱,尤其是中缝核可能会导致这种过度兴奋。本研究旨在调查大中缝核 (NRM) 在 MOH 大鼠模型中皮层和三叉神经过度兴奋的发展中的参与。结果 对乙酰氨基酚的长期治疗增加了皮层扩散抑制 (CSD) 的频率和 c 的数量-三叉神经尾核 (TNC) 中的 Fos 免疫反应 (Fos-IR) 神经元。在对照组中,显微注射到 NRM 中的 muscimol 显着增加了 TNC 中 CSD 诱发的直流偏移和 Fos-IR 神经元的频率。在长期接触对乙酰氨基酚的大鼠中未发现这种促进作用。在静脉全身输注硝酸甘油 (NTG) 诱发的偏头痛模型中,与未接受对乙酰氨基酚治疗的大鼠相比,长期接触对乙酰氨基酚的大鼠在 TNC 中表现出更频繁的神经元放电和更大的 Fos-IR。Muscimol 显微注射增加了对照大鼠 TNC 中的神经元放电,但在对乙酰氨基酚治疗的大鼠中没有。TNC中Fos-IR细胞的数量没有显着变化。结论长期接触对乙酰氨基酚会改变NRM的功能,导致皮层过度兴奋和促进三叉神经伤害感受。与未接受对乙酰氨基酚治疗的大鼠相比,长期接触对乙酰氨基酚的大鼠在 TNC 中表现出更频繁的神经元放电和更大的 Fos-IR。Muscimol 显微注射增加了对照大鼠 TNC 中的神经元放电,但在对乙酰氨基酚治疗的大鼠中没有。TNC中Fos-IR细胞的数量没有显着变化。结论长期接触对乙酰氨基酚会改变NRM的功能,导致皮层过度兴奋和促进三叉神经伤害感受。与未接受对乙酰氨基酚治疗的大鼠相比,长期接触对乙酰氨基酚的大鼠在 TNC 中表现出更频繁的神经元放电和更大的 Fos-IR。Muscimol 显微注射增加了对照大鼠 TNC 中的神经元放电,但在对乙酰氨基酚治疗的大鼠中没有。TNC中Fos-IR细胞的数量没有显着变化。结论长期接触对乙酰氨基酚会改变NRM的功能,导致皮层过度兴奋和促进三叉神经伤害感受。
更新日期:2019-10-21
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