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在戊巴比妥麻醉的大鼠中,脊髓δ2阿片受体而非δ1、μ或κ阿片受体参与中缝隐核β-内啡肽诱导的甩尾抑制。

Spinal delta 2-, but not delta 1-, mu-, or kappa-opioid receptors are involved in the tail-flick inhibition induced by beta-endorphin from nucleus raphe obscurus in the pentobarbital-anesthetized rat.

作者信息

Tseng L F, Tsai J H, Collins K A, Portoghese P S

机构信息

Department of Anesthesiology, Medical College of Wiscdonsin, Milwaukee 53226, USA.

出版信息

Eur J Pharmacol. 1995 Apr 24;277(2-3):251-6. doi: 10.1016/0014-2999(95)00084-x.

Abstract

The antinociception induced by beta-endorphin given supraspinally has been previously demonstrated to be mediated by the release of [Met5]enkephalin acting on delta-opioid receptors in the spinal cord. The present study was designed to determine what type of opioid receptors in the spinal cord is involved in beta-endorphin-induced antinociception in the rat. Antinociception was induced by beta-endorphin (0.6 nmol) given into nucleus raphe obscurus and was assessed by the tail-flick test in pentobarbital-anesthesized rats. Naltriben (0.6-6.0 nmol), a selective delta 2-opioid receptor antagonist, given intrathecally dose-dependently attenuated beta-endorphin-induced inhibition of the tail-flick response. On the other hand, 7-benzylidene naltrexone (2.1-64.3 nmol), CTOP (D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2, 0.09-2.8 nmol), or nor-binaltorphimine (1.4-40.8 nmol), selective delta 1-, mu-, and kappa-opioid receptor antagonists, respectively, did not block beta-endorphin-induced antinociception. The results of present study in rats are consistent with previous experiments in mice indicating that spinal delta 2-, but not delta 1-, mu- or kappa-opioid receptors are involved in beta-endorphin-induced inhibition of the tail-flick response.

摘要

先前已证明,脑啡肽在脊髓以上水平给予时所诱导的抗伤害感受是由[Met5]脑啡肽的释放介导的,该脑啡肽作用于脊髓中的δ阿片受体。本研究旨在确定脊髓中何种类型的阿片受体参与β-内啡肽诱导的大鼠抗伤害感受。通过向中缝隐核注射β-内啡肽(0.6 nmol)诱导抗伤害感受,并在戊巴比妥麻醉的大鼠中通过甩尾试验进行评估。鞘内注射选择性δ2阿片受体拮抗剂纳曲苄(0.6 - 6.0 nmol)可剂量依赖性地减弱β-内啡肽诱导的甩尾反应抑制。另一方面,选择性δ1、μ和κ阿片受体拮抗剂7-亚苄基纳曲酮(2.1 - 64.3 nmol)、CTOP(D-苯丙氨酸-半胱氨酸-酪氨酸-D-色氨酸-鸟氨酸-苏氨酸-苯丙氨酸-苏氨酸-NH2,0.09 - 2.8 nmol)或去甲二丙诺啡(1.4 - 40.8 nmol)均未阻断β-内啡肽诱导的抗伤害感受。本研究在大鼠中的结果与先前在小鼠中的实验一致,表明脊髓中的δ2阿片受体而非δ1、μ或κ阿片受体参与β-内啡肽诱导的甩尾反应抑制。

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