Glial cells and chronic pain.
Glial cells and chronic pain.
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DOI：
10.1177/1073858409360822
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发表时间：
2010-10
期刊：
影响因子：
--
通讯作者：
Decosterd I
中科院分区：
文献类型：
--
作者：
Gosselin RD;Suter MR;Ji RR;Decosterd I
在过去的几年里，神经胶质细胞对疼痛的控制已经成为对抗病理性疼痛的一个有希望的靶点。事实上，神经胶质表型的变化已经在整个伤害性通路中报道，从外周神经到更高的整合性脑区域，并且这种神经胶质反应的药理学抑制减少了动物模型中疼痛的表现。神经胶质和神经元之间的这种复杂的相互作用依赖于各种机制，这取决于所考虑的神经胶质细胞类型（星形胶质细胞、小胶质细胞、卫星细胞或许旺细胞）、调节过程的解剖位置（外周神经、脊髓或脑）以及慢性疼痛范例的性质。在细胞内，最近的进展已经指出了特定级联的激活，例如在神经胶质激活背后的潜在过程中的促分裂原相关蛋白激酶（MAPK）。此外，由于神经胶质细胞完成的大量功能，各种机制可能使伤害感受神经元敏感，包括释放原伤害感受细胞因子和神经营养因子或改变神经递质清除能力。作者回顾了近年来关于中枢和外周胶质细胞在慢性疼痛动物模型中的意义的概念进展，并讨论了将来将其转化为人类治疗的可能性。
Over the past few years, the control of pain exerted by glial cells has emerged as a promising target against pathological pain. Indeed, changes in glial phenotypes have been reported throughout the entire nociceptive pathway, from peripheral nerves to higher integrative brain regions and pharmacological inhibition of such glial reactions reduces the manifestation of pain in animal models. This complex interplay between glia and neurons relies on various mechanisms depending both on glial cell types considered (astrocytes, microglia, satellite cells or Schwann cells), the anatomical location of the regulatory process (peripheral nerve, spinal cord or brain) and the nature of the chronic pain paradigm. Intracellularly, recent advances have pointed out to the activation of specific cascades, such as mitogen associated protein kinases (MAPK) in the underlying processes behind glial activation. In addition, given the large number of functions accomplished by glial cells, various mechanisms might sensitize nociceptive neurons including a release of pronociceptive cytokines and neurotrophins or changes in neurotransmitter scavenging capacity. The authors review the conceptual advances made in the recent years about the implication of central and peripheral glia in animal models of chronic pain and discuss the possibility to translate it into human therapies in the future.
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影响因子：
15.1
作者：
Dublin, Pavel;Hanani, Menachem
通讯作者：
Hanani, Menachem
影响因子：
7.4
作者：
Chudler, EH;Anderson, LC;Byers, MR
通讯作者：
Byers, MR
影响因子：
3
作者：
Brisby, H;Olmarker, K;Rydevik, B
通讯作者：
Rydevik, B
影响因子：
5.3
作者：
Colburn, RW;Rickman, AJ;DeLeo, JA
通讯作者：
DeLeo, JA
影响因子：
3.3
作者：
Holdridge, Sarah V.;Armstrong, Stacey A.;Taylor, Anna M. W.;Cahill, Catherine M.
通讯作者：
Cahill, Catherine M.