Involvement of trigeminal astrocyte activation in masseter hyperalgesia under stress

Involvement of trigeminal astrocyte activation in masseter hyperalgesia under stress
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三叉神经星形胶质细胞活化参与应激下咬肌痛觉过敏

DOI:
10.1016/j.physbeh.2015.02.005
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发表时间:
2015-04
影响因子:
2.9
通讯作者:
Chen, Yong-Jin
Chen, Yong-Jin
中科院分区:
医学3区
文献类型:
--
作者:
Zhao, Yin-Hua;Wang, Jian;Zhang, Min;Chen, Yong-Jin

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人们普遍认为,心理压力会导致颞下颌关节紊乱,其中慢性口面部疼痛是主要症状。然而,这些疾病发生的核心机制仍不清楚。目前的研究旨在确定三叉神经尾部亚核中的神经胶质细胞在应激引起的大鼠咬肌痛觉过敏增加中的参与。在遭受慢性束缚应激后,动物表现出体重增加减少、行为改变和明显的咬肌异常疼痛。我们还发现,三叉神经尾亚核(Vc)中的星形胶质细胞(而非小胶质细胞)被显着激活。进行了进一步的分析以调查神经胶质细胞的贡献;我们向应激大鼠鞘内注射l-α-氨基己二酸(星形胶质细胞特异性抑制剂)和/或米诺环素(小胶质细胞特异性抑制剂)。我们的结果表明,l-α-氨基己二酸(LAA),但不是米诺环素,可以显着减轻由约束应激引起的机械咬肌异常性疼痛和行为变化。此外,慢性束缚应激后,Vc中白细胞介素-1β(IL-1β)和磷酸化N-甲基-d-天冬氨酸受体1(p-NR1)的表达显着增加,而LAA则显着抑制IL-1β和p-NR1的过度表达。综上所述,这些结果表明,Vc 中活化的星形胶质细胞可能是约束应激引起的咬肌痛觉过敏病理生理学中最重要的因素之一,随后的 IL-1β 过度表达和过度的 NMDAR 磷酸化可能最终导致咬肌痛觉过敏。因此,抑制脊髓星形细胞活化可能代表治疗压力引起的口面部疼痛的新治疗策略。
It is commonly accepted that psychological stress contributes to the development of temporomandibular joint disorders, in which chronic orofacial pain is the main symptom. However, the central mechanism underlying the development of these disorders has remained unclear. The current study was performed to determine the involvement of the glia in the trigeminal spinal subnucleus caudalis in stress-induced increases in masseter muscle hyperalgesia in rats. After being subjected to chronic restraint stress, the animals showed decreased body weight gain, behavioral changes and marked masseter allodynia. We also found that astrocytes, but not microglia, in the trigeminal subnucleus caudalis (Vc) were dramatically activated. A further analysis was undertaken to investigate the contribution of the glia; we intrathecally injectedl-α-aminoadipate (astrocyte-specific inhibitor) and/or minocycline (microglia-specific inhibitor) into the stressed rats. Our results showed thatl-α-aminoadipate (LAA), but not minocycline, could significantly attenuate the mechanical masseter allodynia and behavioral changes induced by restraint stress. In addition, the expression of interleukin-1β (IL-1β) and phosphorylated N-methyl-d-aspartic acid receptor 1 (p-NR1) in the Vc was significantly increased after chronic restraint stress, whereas LAA dramatically inhibited the overexpression of IL-1β and p-NR1. Taken together, these results suggest that activated astrocytes in the Vc may be one of the most important factors in the pathophysiology of masseter hyperalgesia induced by restraint stress and the following overexpression of IL-1β and excessive NMDAR phosphorylation may ultimately contribute to masseter hyperalgesia. Thus, inhibiting spinal astrocytic activation may represent a novel therapeutic strategy for the treatment of orofacial pain induced by stress.
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发表时间: 2013-11
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作者:
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DOI: 10.1523/jneurosci.3365-09.2009
发表时间: 2009-09-09
期刊: The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子: --
作者:
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