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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >p38 mitogen-activated protein kinase is activated after a spinal nerve ligation in spinal cord microglia and dorsal root ganglion neurons and contributes to the generation of neuropathic pain.
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p38 mitogen-activated protein kinase is activated after a spinal nerve ligation in spinal cord microglia and dorsal root ganglion neurons and contributes to the generation of neuropathic pain.

机译：脊髓小胶质细胞和背根神经节神经元中的脊髓神经结扎后，p38丝裂原活化的蛋白激酶被激活，并有助于神经性疼痛的产生。

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摘要

The possible involvement of p38 mitogen-activated protein kinase activation in spinal cord and dorsal root ganglion (DRG) cells in the development of peripheral neuropathic pain has been explored. Ligation of the L5 spinal nerve (SNL) on one side in adult rats produces an early onset and long-lasting mechanical allodynia. This lesion results in activation of p38 in the L5 segment of the spinal cord, most prominently in the ipsilateral dorsal horn, starting soon after the lesion (<1 d) and persisting for >3 weeks. The activated p38 in the spinal cord is restricted entirely to microglia; phospho-p38 colocalizes only with the microglial marker OX-42 and not with either the neuronal marker neuronal-specific nuclear protein or the astrocyte marker GFAP. In contrast, SNL induces a delayed (>3 d) activation of p38 in the L5 DRG that occurs predominantly in neurons. Continuous injection of the p38 inhibitor 4-(4-fluorophenyl)-2-(4-methylsulfonylphenyl)-5-(4-pyridyl)-1H-imidazole (SB203580) via the intrathecal route, starting before the SNL surgery, reduces SNL-induced mechanical allodynia from day 1 to day 10, with maximal effects at early time points. Post-treatment with SB203580 starting on day 1 or on day 10 after surgery also reduces established mechanical allodynia. Because the reduction in neuropathic pain by p38 inhibition occurs before the appearance of p38 activation in DRG neurons, p38 activation in spinal cord microglia is likely to have a substantial role in the earliest phase of neuropathic pain. Coactivation of p38 in DRG neurons and spinal microglia may contribute to later phases of neuropathic pain.
机译：已经探讨了p38丝裂原活化蛋白激酶激活在脊髓和背根神经节（DRG）细胞中可能参与周围神经性疼痛的发展。成年大鼠一侧的L5脊神经（SNL）结扎可导致早期发作和持久的机械性异常性疼痛。这种病变导致脊髓L5段中p38的激活，最明显的是在同侧背角，在病变后不久（<1 d）开始并持续> 3周。脊髓中激活的p38完全局限于小胶质细胞;磷酸化-p38仅与小胶质细胞标记物OX-42共定位，而与神经元标记物神经元特异性核蛋白或星形胶质细胞标记物GFAP不共定位。相反，SNL诱导L5 DRG中p38的激活延迟（> 3 d），这主要发生在神经元中。在SNL手术之前开始，通过鞘内途径连续注射p38抑制剂4-（4-氟苯基）-2-（4-甲基磺酰基苯基）-5-（4-吡啶基）-1H-咪唑（SB203580），可降低SNL-从第1天到第10天诱发机械性异常性疼痛，并在早期时间点发挥最大作用。在手术后的第1天或第10天开始用SB203580进行后处理也可以减少既定的机械性异常性疼痛。由于通过p38抑制减轻神经性疼痛的发生发生在DRG神经元中出现p38激活之前，因此脊髓小胶质细胞中p38的激活可能在神经性疼痛的最早阶段起着重要作用。 DRG神经元和脊髓小胶质细胞中p38的共激活可能有助于神经性疼痛的后期阶段。

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