• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular pain >Role of spinal P2Y6 and P2Y11 receptors in neuropathic pain in rats: possible involvement of glial cells
【24h】

Role of spinal P2Y6 and P2Y11 receptors in neuropathic pain in rats: possible involvement of glial cells

机译：脊髓P2Y 6 和P2Y 11 受体在大鼠神经性疼痛中的作用：胶质细胞可能参与

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Background The participation of spinal P2X receptors in neuropathic pain is well recognized. However, the role of P2Y receptors has been less studied. The purpose of this study was to investigate the contribution of spinal P2Y6,11 receptors following peripheral nerve damage induced by spinal nerve ligation. In addition, we determined the expression of P2Y6,11 receptors in the dorsal spinal cord in presence of the selective P2Y6,11 receptors antagonists. Furthermore, we evaluated the participation of spinal microglia and astrocytes in the pronociceptive role of P2Y6,11 receptors. Results Spinal administration of the selective P2Y6 (MRS2578, 10–100 μM) and P2Y11 (NF340, 0.3–30 μM) receptor antagonists reduced tactile allodynia in spinal nerve ligated rats. Nerve injury increased the expression of P2Y6,11 receptors at 7, 14 and 21 days after injury. Furthermore, intrathecal administration of MRS2578 (100 μM/day) and NF340 (30 μM/day) for 3 days significantly reduced spinal nerve injury-induced increase in P2Y6,11 receptors expression, respectively. Spinal treatment (on day 14 after injury) with minocycline (100 μg/day) or fluorocitrate (1 nmol/day) for 7 days reduced tactile allodynia and spinal nerve injury-induced up-regulation in Iba-1 and GFAP, respectively. In addition, minocycline reduced nerve injury-induced up-regulation in P2Y6,11 receptors whereas that fluorocitrate diminished P2Y11, but not P2Y6, receptors up-regulation. Intrathecal treatment (on day 21 after injury) with the selective P2Y6 (PSB0474, 3–30 μM) and P2Y11 (NF546, 1–10 μM) receptor agonists produced remarkable tactile allodynia in nerve ligated rats previously treated with minocycline or fluorocitrate for 7 days. Conclusions Our data suggest that spinal P2Y6 is present in spinal microglia while P2Y11 receptors are present in both spinal microglia and astrocytes, and both receptors are up-regulated in rats subjected to spinal nerve injury. In addition, our data suggest that the spinal P2Y6 and P2Y11 receptors participate in the maintenance of neuropathic pain.
机译：背景脊髓P2X受体参与神经性疼痛已广为人知。但是，对P2Y受体的作用研究较少。这项研究的目的是调查脊髓神经结扎引起的周围神经损伤后脊髓P2Y6，11受体的贡献。此外，我们确定了在存在选择性P2Y6,11受体拮抗剂的情况下背脊髓中P2Y6,11受体的表达。此外，我们评估了脊髓小胶质细胞和星形胶质细胞参与P2Y6,11受体的伤害感受作用。结果脊髓施用选择性P2Y6（MRS2578，10–100μM）和P2Y11（NF340，0.3–30μM）受体拮抗剂可减轻结扎脊髓神经的大鼠的触觉异常性疼痛。神经损伤在损伤后第7、14和21天增加P2Y6,11受体的表达。此外，鞘内给予MRS2578（100μM/天）和NF340（30μM/天）3天，分别显着降低了脊髓神经损伤引起的P2Y6,11受体表达增加。用米诺环素（100μg/天）或氟柠檬酸盐（1 nmol /天）进行7天的脊柱治疗（受伤后第14天），分别降低了Iba-1和GFAP的触觉异常性疼痛和脊神经损伤引起的上调。此外，米诺环素减少了P2Y6,11受体引起的神经损伤诱导的上调，而氟柠檬酸减少了P2Y11受体的上调，但不减少P2Y6受体的上调。鞘内使用选择性P2Y6（PSB0474，3–30μM）和P2Y11（NF546，1–10μM）受体激动剂鞘内治疗（损伤后第21天），可在神经结扎大鼠中预先用米诺环素或氟柠檬酸治疗7天，产生明显的触觉异常性疼痛。 。结论我们的数据表明，脊髓小胶质细胞中存在脊髓P2Y6，而脊髓小胶质细胞和星形胶质细胞中均存在P2Y11受体，并且在脊髓神经损伤大鼠中这两种受体均上调。此外，我们的数据表明，脊髓P2Y6和P2Y11受体参与了神经性疼痛的维持。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号