• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Analgesia induced by 2- or 100-Hz electroacupuncture in the rat tail-flick test depends on the anterior pretectal nucleus
【24h】

Analgesia induced by 2- or 100-Hz electroacupuncture in the rat tail-flick test depends on the anterior pretectal nucleus

机译：大鼠甩尾试验中2或100 Hz电针所引起的镇痛取决于前额棘前核

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

Aims The anterior pretectal nucleus (APtN) and electroacupuncture (EA) activate descending mechanisms to modulate nociceptive inputs in the spinal dorsal horn. This study examines qualitatively whether mechanisms in the APtN participate in the EA-induced analgesia in rats. Main methods The tail-flick test was utilized to examine the changes produced by non-selective antagonists of serotonergic (methysergide, 37 pg), muscarinic (atropine, 10 ng) and opioid (naloxone, 10 ng) receptors; selective antagonists against μ (CTOP, 6.4 μg), δ (ICI174,864, 6.9 μg) or κ (nor-BNI, 7.3 μg); 5HT1 (methiothepin, 0.47 μg), 5HT2 (ketanserin, 5.4 μg), or 5HT3 (MDL 72222, 15.7 μg); and GABAA (bicuculline, 150 ng) receptors injected into the dorsal (d) or ventral (v) APtN on the antinociception induced by a 20-min EA applied at 2- or 100-Hz frequency to the Zusanli and Sanyinjiao acupoints. Key findings The 2-Hz EA-induced analgesia was blocked by naloxone, CTOP or atropine, was less intense after bicuculline, was shorter after methysergide or methiothepin in dAPtN, and was less intense after methysergide, methiothepin and bicuculline in vAPtN. The 100-Hz EA-induced analgesia was less intense after methysergide, methiothepin and CTOP in vAPtN, and remained unchanged after injection of the antagonists into the dAPtN. Significance The 2-Hz EA-induced analgesia utilizes cholinergic muscarinic, μ-opioid, GABAA and 5-HT1 mechanisms in the dAPtN and μ-opioid and 5-HT1 mechanisms in the vAPtN, while 100-Hz EA-induced analgesia utilizes μ-opioid and 5-HT1 mechanisms in the vAPtN but does not utilize them in the dAPtN.
机译：目的前直肠前核（APtN）和电针（EA）激活下降机制来调节脊髓背角的伤害性输入。这项研究定性地检查了APtN中的机制是否参与了EA诱导的大鼠镇痛。主要方法用甩尾试验检查非选择性拮抗剂对血清素能（甲基麦角酰胺，37 pg），毒蕈碱（阿托品，10 ng）和阿片样物质（纳洛酮，10 ng）受体产生的变化。针对μ（CTOP，6.4μg），δ（ICI174,864，6.9μg）或κ（nor-BNI，7.3μg）的选择性拮抗剂; 5HT1（甲氧西平，0.47μg），5HT2（酮色林，5.4μg）或5HT3（MDL 72222，15.7μg）;以及将20分钟的EA以2或100 Hz频率施加于足三里穴和三阴交穴的抗伤害感受后，将GABAA（小核蛋白，150 ng）的背侧（d）或腹侧（v）的APtN注射。关键发现2 Hz EA诱导的镇痛作用被纳洛酮，CTOP或阿托品阻滞，在双小分子后在dAPtN中强度较弱，在dAPtN中的美塞麦肽或Methiothepin后较短，在vAPtN中的美西麦角，Methiothepin和Bicuculline后强度较弱。在vAPtN中加入美塞麦肽，Methiothepin和CTOP后，以100 Hz EA诱导的镇痛作用减弱，在将拮抗剂注入dAPtN中后保持不变。意义2 Hz EA诱导的镇痛利用dAPtN中的胆碱能毒蕈碱，μ阿片类药物，GABAA和5-HT1机制，而vAPtN则利用μ阿片类药物和5-HT1机制，而100 Hz EA诱导的镇痛利用μ- vAPtN中的阿片类药物和5-HT1机制，但在dAPtN中没有利用它们。

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