...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Contribution of spinal inhibitory receptors in heterosegmental antinociception induced by noxious stimulation.
【24h】

Contribution of spinal inhibitory receptors in heterosegmental antinociception induced by noxious stimulation.

机译：脊柱抑制性受体在有毒刺激诱导的异节性抗伤害感受中的作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Noxious (i.e. painful) stimulation in the rat induces profound heterosegmental antinociception as demonstrated by the ability of either thermal stimulation (50 degrees C water) or subdermal capsaicin injection in the hindpaw to attenuate the nociceptive trigeminal jaw-opening reflex. Importantly, noxious stimulus-induced antinociception (NSIA) is mediated by endogenous opioids (as well as other neurotransmitters) in nucleus accumbens, as indicated by the ability of intra-accumbens administration of mu- or delta-opioid receptor antagonists to block NSIA. Although noxious peripheral stimulation is known to release excitatory neurotransmitters such as glutamate at the level of the spinal cord, the present study was designed to test the hypothesis that NSIA depends on further activation of spinal inhibitory receptors. This hypothesis was based on findings that inhibition of spinal processing (e.g. intrathecal local anaesthetic administration) also produces heterosegmental antinociception mediated by endogenous opioids in nucleus accumbens. Thus, to reconcile the paradoxical findings that both spinal excitation and inhibition appear to activate the same nucleus accumbens opioid-mediated antinociceptive mechanism, we investigated whether spinal administration of antagonists for inhibitory receptors would block the antinociceptive effect of subdermal capsaicin. We report that spinal administration of selective antagonists for mu-opioid (Cys2, Tyr3, Orn5, Pen7amide), kappa-opioid (nor-binaltorphimine), GABA-A (bicuculline), GABA-B (CGP 35348) and glycine (strychnine) receptors significantly reduced NSIA. The selective delta-opioid receptor antagonist naltrindole had no significant effect. These results, together with our previous findings, suggest that peripheral noxious stimuli release endogenous opioids, GABA and glycine in the spinal cord which, in turn, inhibit tonic pronociceptive spinal activity to produce heterosegmental antinociception mediated in nucleus accumbens.
机译：大鼠中的有害（即疼痛）刺激可诱发深层的异段性痛觉感受，如热刺激（50度水）或后足皮下注射辣椒素的能力减弱了伤害性三叉神经下颌开放性反射的能力所证明。重要的是，伏隔核中的内源性阿片类药物（以及其他神经递质）介导了有害刺激诱导的抗伤害感受（NSIA），如通过伏打内给予mu或delta阿片类受体拮抗剂阻断NSIA的能力所表明。尽管已知有害的周围刺激会在脊髓水平上释放出兴奋性神经递质，例如谷氨酸，但本研究的目的是检验以下假设：NSIA依赖于脊髓抑制性受体的进一步激活。该假设基于以下发现：抑制脊柱加工（例如鞘内局部麻醉）也会产生伏隔核内源性阿片类药物介导的异段抗伤害感受。因此，为了调和矛盾的发现，即脊柱兴奋和抑制似乎都激活了相同的伏隔核阿片介导的抗伤害感受机制，我们调查了脊柱给予抑制受体拮抗剂的拮抗剂是否会阻断皮下辣椒素的抗伤害感受。我们报告说，对μ阿片类药物（Cys2，Tyr3，Orn5，Pen7amide），κ阿片类药物（nor-binaltorphimine），GABA-A（比库洛林），GABA-B（CGP 35348）和甘氨酸（司亭宁）进行选择性拮抗剂的脊髓给药受体显着降低NSIA。选择性δ-阿片受体拮抗剂纳曲酮没有明显作用。这些结果，加上我们以前的发现，表明周围的有害刺激物在脊髓中释放出内源性阿片样物质，GABA和甘氨酸，进而抑制滋补性伤害感受性脊髓活性，从而产生伏隔核介导的异段抗伤害感受。

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