Glial contributions to visceral pain: implications for disease etiology and the female predominance of persistent pain.

Glial contributions to visceral pain: implications for disease etiology and the female predominance of persistent pain.
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DOI:
10.1038/tp.2016.168
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发表时间:
2016-09-13
影响因子:
6.8
通讯作者:
Hutchinson MR
Hutchinson MR
中科院分区:
医学1区
文献类型:
--
作者:
Dodds KN;Beckett EA;Evans SF;Grace PM;Watkins LR;Hutchinson MR

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在中枢神经系统中,神经胶质细胞和神经元之间的双向信号传导(“神经免疫通讯”)促进了持续性疼痛的发展。脊髓胶质细胞可以通过延长神经因子信号的释放,使邻近的中央投射神经元敏感,从而促进疼痛状态的加剧。尽管许多持续性疼痛在女性中非常常见,但是否特定的神经免疫机制导致了这种易感性的增加尚不清楚。这篇综述总结了神经胶质细胞和神经免疫相互作用在疼痛中的主要已知贡献,主要是在雄性啮齿动物和躯体疼痛条件下确定的。因此,研究女性常见内脏疾病引起的疼痛的神经免疫相互作用可能为研究女性疼痛的独特机制提供更合适的途径。此外,我们讨论了潜在的脊髓胶质细胞和随后的神经源性炎症作为外周炎症发展的一个促进因素,因此,代表了女性发展出高比例的这种持续疼痛状况的易感因素。
In the central nervous system, bidirectional signaling between glial cells and neurons (‘neuroimmune communication') facilitates the development of persistent pain. Spinal glia can contribute to heightened pain states by a prolonged release of neurokine signals that sensitize adjacent centrally projecting neurons. Although many persistent pain conditions are disproportionately common in females, whether specific neuroimmune mechanisms lead to this increased susceptibility remains unclear. This review summarizes the major known contributions of glia and neuroimmune interactions in pain, which has been determined principally in male rodents and in the context of somatic pain conditions. It is then postulated that studying neuroimmune interactions involved in pain attributed to visceral diseases common to females may offer a more suitable avenue for investigating unique mechanisms involved in female pain. Further, we discuss the potential for primed spinal glia and subsequent neurogenic inflammation as a contributing factor in the development of peripheral inflammation, therefore, representing a predisposing factor for females in developing a high percentage of such persistent pain conditions.
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