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鞘内注射β-内啡肽诱导的甩尾抑制是由小鼠体内κ-和μ-阿片受体的激活介导的。

The tail-flick inhibition induced by beta-endorphin administered intrathecally is mediated by activation of kappa- and mu-opioid receptors in the mouse.

作者信息

Tseng L F, Collins K A

机构信息

Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee 53226.

出版信息

Eur J Pharmacol. 1992 Apr 7;214(1):59-65. doi: 10.1016/0014-2999(92)90096-m.

Abstract

The inhibition of the tail-flick response induced by beta-endorphin given i.c.v. has been demonstrated to be mediated by the stimulation of epsilon- but not mu-, delta- or kappa-opioid receptors. beta-Endorphin given i.t. also inhibited the tail-flick response. The present studies were designed to determine what types of opioid receptors in the spinal cord were involved in i.t. beta-endorphin-induced tail-flick inhibition. Blockade of kappa-opioid receptors by coadministration of nor-binaltorphimine or Win 44,441-3 with beta-endorphin given i.t. dose dependently inhibited i.t. beta-endorphin-induced inhibition of the tail-flick response. Blockade of mu-opioid receptors by i.t. coadministration of D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH2 with beta-endorphin blocked i.t. beta-endorphin-induced inhibition of the tail-flick response. I.t. injection of delta-opioid receptors antagonists, ICI 174,864 and naltrindole, or epsilon-opioid receptor antagonist, beta-endorphin-(1-27), did not affect inhibition of the tail-flick response induced by beta-endorphin given i.t. Blockade of alpha 2-adrenoceptors and 5-HT receptors by i.t. injection of yohimbine and methysergide, respectively, also did not affect inhibition of the tail-flick response induced by beta-endorphin given i.t. The results indicate that the inhibition of the tail-flick response induced by beta-endorphin given i.t. is mediated by the stimulation of kappa- and mu-opioid receptors but not delta- and epsilon-opioid receptors, alpha 2-adrenoceptors or 5-HT receptors.

摘要

脑室内注射β-内啡肽所诱导的甩尾反应抑制已被证明是由刺激ε-阿片受体介导的,而非μ-、δ-或κ-阿片受体。鞘内注射β-内啡肽也能抑制甩尾反应。本研究旨在确定脊髓中何种类型的阿片受体参与了鞘内注射β-内啡肽所诱导的甩尾抑制。将去甲二氢吗啡酮或Win 44,441-3与鞘内注射的β-内啡肽共同给药以阻断κ-阿片受体,可剂量依赖性地抑制鞘内注射β-内啡肽所诱导的甩尾反应抑制。将D-苯丙氨酸-半胱氨酸-酪氨酸-D-色氨酸-鸟氨酸-苏氨酸-青霉胺-苏氨酸-酰胺与鞘内注射的β-内啡肽共同给药以阻断μ-阿片受体,可阻断鞘内注射β-内啡肽所诱导的甩尾反应抑制。鞘内注射δ-阿片受体拮抗剂ICI 174,864和纳曲吲哚,或ε-阿片受体拮抗剂β-内啡肽-(1-27),并不影响鞘内注射β-内啡肽所诱导的甩尾反应抑制。分别通过鞘内注射育亨宾和麦角新碱阻断α2-肾上腺素能受体和5-羟色胺受体,也不影响鞘内注射β-内啡肽所诱导的甩尾反应抑制。结果表明,鞘内注射β-内啡肽所诱导的甩尾反应抑制是由κ-和μ-阿片受体的刺激介导的,而非δ-和ε-阿片受体、α2-肾上腺素能受体或5-羟色胺受体。

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