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在机械性或热性伤害性刺激后,大鼠背角中δ-阿片受体对P物质样免疫反应性释放的调节作用。

Delta-Opioid receptor modulation of the release of substance P-like immunoreactivity in the dorsal horn of the rat following mechanical or thermal noxious stimulation.

作者信息

Zachariou V, Goldstein B D

机构信息

Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta 30912-7605, USA.

出版信息

Brain Res. 1996 Oct 14;736(1-2):305-14. doi: 10.1016/0006-8993(96)00718-4.

Abstract

The present study was undertaken to investigate the effects of the opioid peptide Met-enkephalin (met-enk) on the release of substance P-like immunoreactivity (SPLI) in the lumbar dorsal horn during the application of a noxious mechanical or thermal stimulus to the ipsilateral hind paw and lower limb of the rat. A push-pull cannula was introduced to the lumbar dorsal horn in non-anesthetized decerebrate/spinal transected rats. The dorsal horn was perfused with artificial CSF and the collected perfusates were assayed for SPLI using radioimmunoassay. A noxious mechanical or thermal stimulus was applied to different areas of the ipsilateral hind paw and lower limb. Met-enk (500 nM) applied to the dorsal horn through the perfusate reduced the basal release of SPLI by 29 +/- 9% and prevented the increase in the release of SPLI evoked by the noxious mechanical or thermal stimulus. The effect of met-enk was blocked by the selective delta-opioid receptor antagonist naltrindole (500 nM). Naltrindole (NTD) alone elicited a 75 +/- 30% increase in the basal release of SPLI. These data show that met-enk inhibits the thermally or mechanically evoked release of SPLI in the dorsal horn by activating the delta opioid receptors. These receptors are also involved in the tonic spinal regulation of the release of SPLI.

摘要

本研究旨在探讨阿片肽甲硫氨酸脑啡肽(met-enk)在对大鼠同侧后爪和下肢施加有害机械或热刺激时,对腰髓背角P物质样免疫反应性(SPLI)释放的影响。在未麻醉的去大脑/脊髓横断大鼠的腰髓背角插入一个推挽式套管。背角用人工脑脊液灌流,收集的灌流液用放射免疫分析法检测SPLI。对同侧后爪和下肢的不同部位施加有害机械或热刺激。通过灌流液将met-enk(500 nM)施加到背角,可使SPLI的基础释放减少29±9%,并阻止有害机械或热刺激引起的SPLI释放增加。met-enk的作用被选择性δ阿片受体拮抗剂纳曲吲哚(500 nM)阻断。单独使用纳曲吲哚(NTD)可使SPLI的基础释放增加75±30%。这些数据表明,met-enk通过激活δ阿片受体抑制背角中热或机械诱发的SPLI释放。这些受体也参与了SPLI释放的脊髓紧张性调节。

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