Spinal p38 mitogen-activated protein kinase mediates allodynia induced by first-degree burn in the rat.
Spinal p38 mitogen-activated protein kinase mediates allodynia induced by first-degree burn in the rat.
复制标题
DOI：
10.1002/jnr.21905
复制
发表时间：
2009-03
影响因子：
4.2
通讯作者：
Campana, W. Marie
中科院分区：
文献类型：
--
作者：
Sorkin, Linda;Svensson, Camilla I.;Jones-Cordero, Toni L.;Hefferan, Michael P.;Campana, W. Marie
脊髓中p38 MAP激酶（MAPK）的激活与疼痛状态的发展和维持有关。在这项研究中，我们测试了p38 MAPK是否参与了对后爪一度烧伤的反应。这种损伤诱导中枢敏感化，导致触觉异常性疼痛，通过PKC和PKA激活Ca 2+渗透性AMPA/红藻氨酸受体介导。我们证明，p38 MAPK是迅速和强大的激活后，在浅脊髓背角轻度热损伤后，后爪。激活的p38 MAPK主要定位于小胶质细胞，少突胶质细胞和第二层神经元在较小程度上。星形胶质细胞不参与p38 MAPK反应。鞘内预处理p38 MAPK的药理学抑制剂（SB 203580，SD-282）剂量依赖性地阻断触觉异常性疼痛的发展，这是一度烧伤模型的特征。当它们在损伤后给药时，抑制剂对触觉异常性疼痛的作用丧失。这些研究确定p38 MAPK作为触觉异常性疼痛的主要介质，最有可能在AMPA/红藻氨酸受体下游激活。
Activation of p38 MAP kinase (MAPK) in the spinal cord has been implicated in the development and maintenance of pain states. In this study, we tested whether p38 MAPK is involved in the response to first-degree burn of the hindpaw. This injury induces central sensitization leading to tactile allodynia, mediated by activation of Ca2+ permeable AMPA/kainate receptors through PKC and PKA. We demonstrate that p38 MAPK is rapidly and robustly activated in the superficial spinal dorsal horn after mild thermal injury to the hindpaw. Activated p38 MAPK was localized primarily to microglia and to a lesser extent in oligodendrocytes and lamina II neurons. Astrocytes were not involved in the p38 MAPK response. Intrathecal pretreatment of pharmacological inhibitors of p38 MAPK (SB203580, SD-282) dose-dependently blocked development of tactile allodynia, a characteristic of the first-degree burn model. The effects of the inhibitors on tactile allodynia were lost when they were administered post-injury. These studies identify p38 MAPK as a major mediator of tactile allodynia, most likely activated downstream of AMPA/kainate receptors.
登录
查看更多内容
影响因子：
25
作者：
Ji, RR;Baba, H;Woolf, CJ
通讯作者：
Woolf, CJ
影响因子：
5.3
作者：
Hefferan, Michael P.;Kucharova, Karolina;Marsala, Martin
通讯作者：
Marsala, Martin
DOI：
10.1006/bbrc.1996.1869
发表时间：
1996-12-24
影响因子：
3.1
作者：
Campana, WM;Hiraiwa, M;OBrien, JS
通讯作者：
OBrien, JS
影响因子：
7.4
作者：
Ma, WY;Quirion, R
通讯作者：
Quirion, R
影响因子：
4.7
作者：
Svensson, CI;Marsala, M;Yaksh, TL
通讯作者：
Yaksh, TL