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体内关节炎大鼠脊髓中甲硫氨酸脑啡肽样物质的自发释放和诱发释放。

Spontaneous and evoked release of met-enkephalin-like material from the spinal cord of arthritic rats in vivo.

作者信息

Bourgoin S, Le Bars D, Clot M A, Hamon M, Cesselin F

机构信息

INSERM U 288, Neurobiologie Cellulaire et Fonctionnelle, Faculté de Médecine Pitié-Salpêtrière, 75634 Paris Cedex 13 France INSERM U 161, Neurophysiologie Pharmacologique, 75014 Paris France.

出版信息

Pain. 1988 Jan;32(1):107-114. doi: 10.1016/0304-3959(88)90029-2.

Abstract

Perfusion of the intrathecal space with artificial CSF was achieved in control and arthritic rats under halothane anaesthesia in order to collect the met-enkephalin-like material (MELM) released from the whole spinal cord. On the fourth week following the intradermal injection of Freund's adjuvant to induce arthritis, a marked reduction (-56%) in the spontaneous outflow of MELM was noted in arthritic rats. This effect did not involve changes in the degradation process of MELM, since it persisted when kelatorphan was added to the perfusing fluid in order to inhibit completely the peptidases acting on met-enkephalin. Raising the K+ concentration in the perfusing fluid from 2.4 to 40 mM, as well as moving the hind paws, produced a significant enhancement of MELM release which was (at least) as pronounced in arthritic as in control rats. These results suggest that the basal activity of spinal enkephalinergic neurones, but not that triggered by various stimuli, is reduced in arthritic rats.

摘要

为了收集从整个脊髓释放的甲硫氨酸脑啡肽样物质(MELM),在氟烷麻醉下对对照组和患有关节炎的大鼠进行鞘内人工脑脊液灌注。在皮内注射弗氏佐剂诱导关节炎后的第四周,患有关节炎的大鼠MELM的自发流出量显著减少(-56%)。这种效应与MELM降解过程的变化无关,因为当在灌注液中加入凯托啡以完全抑制作用于甲硫氨酸脑啡肽的肽酶时,该效应仍然存在。将灌注液中的K+浓度从2.4 mM提高到40 mM,以及移动后爪,均使MELM释放显著增强,在患有关节炎的大鼠中(至少)与对照组大鼠一样明显。这些结果表明,患有关节炎的大鼠脊髓脑啡肽能神经元的基础活性降低,但由各种刺激触发的活性未降低。

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