首页> 外文期刊>European Journal of Pharmacology: An International Journal >Functional interactions between delta- and mu-opioid receptors in rat thermoregulation.
【24h】

Functional interactions between delta- and mu-opioid receptors in rat thermoregulation.

机译:大鼠温度调节中的δ-阿片受体和μ-阿片受体之间的功能相互作用。

获取原文
获取原文并翻译 | 示例
           

摘要

The selective delta-opioid receptor agonist deltorphin II (25.0-100.0 microg, i.c.v.) produced biphasic effects on core temperature in rats, in which hypothermia was followed by hyperthermia. Pretreatment with the selective delta-opioid receptor antagonist, naltrindole (25.0 microg, i.c.v.), blocked hypothermia produced by deltorphin II and had a tendency to potentiate the hyperthermic effect of deltorphin II. The non-selective opioid receptor antagonist naloxone (1.5 mg kg(-1), s.c.) potentiated hypothermia, and blocked hyperthermia, produced by deltorphin II (100.0 microg). Also, naloxone potentiated hypothermia produced by a lower dose of deltorphin II (25.0 microg), which did not produce hyperthermia. A similar pattern was found for the selective mu-opioid receptor antagonist, beta-funaltrexamine (5.0 microg, i.c.v.), which potentiated and blocked deltorphin II-induced hypo- and hyperthermia, respectively. The selective kappa-opioid receptor antagonist nor-binaltorphimine (20.0 microg, i.c.v.) had no effects on deltorphin II-induced temperature changes. The present results suggest that deltorphin II produces hypothermia through activation of delta-opioid receptors, whereas the hyperthermic effect of deltorphin II involves activation of mu-opioid receptors. This mu-opioid receptor stimulatory effect of deltorphin II is furthermore more pronounced than was anticipated based on the reported in vitro properties of this compound. The biphasic effect of deltorphin II implies a negative interaction between delta- and mu-opioid receptors in thermoregulation in rats.
机译:选择性δ-阿片样物质受体激动剂deltorphin II(25.0-100.0μg,i.c.v。)对大鼠的核心温度产生双相影响,其中低体温接着是高体温。用选择性δ-阿片受体拮抗剂纳那多尔(25.0μg,i.c.v。)预处理可阻止由deltorphin II产生的体温过低,并倾向于增强deltorphin II的高热作用。非选择性阿片受体拮抗剂纳洛酮(1.5 mg kg(-1),s.c.)增强了体温过低,阻止了德尔托芬II(100.0 microg)产生的体温过高。同样,纳洛酮增强的低温由较低剂量的deltorphin II(25.0 microg)产生,而不会产生高温。发现选择性μ-阿片受体拮抗剂β-富纳曲胺(5.0μg,i.c.v。)具有相似的模式,其分别增强和阻断了deltorphin II引起的体温过低和体温过高。选择性κ-阿片样物质受体拮抗剂去甲双甲托非明(20.0μg,i.c.v。)对deltorphin II诱导的温度变化没有影响。目前的结果表明,deltorphin II通过激活δ阿片受体而产生体温过低,而deltorphin II的高温效应涉及μ阿片受体的激活。与基于已报道的该化合物的体外特性所预期的相比,deltorphin II的这种对阿片受体的刺激作用更加明显。 deltorphin II的双相作用暗示了大鼠温度调节中delta和mu阿片样物质受体之间的负相互作用。

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