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脊髓花生四烯乙醇胺通过体内大麻素受体激活来抑制伤害性感受传递。

Spinal anandamide inhibits nociceptive transmission via cannabinoid receptor activation in vivo.

作者信息

Harris J, Drew L J, Chapman V

机构信息

School of Biomedical Sciences, University of Nottingham Medical School, Queen's Medical Centre, UK.

出版信息

Neuroreport. 2000 Aug 21;11(12):2817-9. doi: 10.1097/00001756-200008210-00041.

DOI:10.1097/00001756-200008210-00041
PMID:10976969
Abstract

The endocannabinoid anandamide has affinity for cannabinoid and vanilloid receptors, which have opposing effects on nociceptive transmission. Effects of spinal administration of anandamide on innocuous and noxious evoked spinal neuronal responses in non-inflamed and carrageenin-inflamed rats were studied. Anandamide (0.1-50 microg/50 microl) had inconsistent effects in non-inflamed rats. Following carrageenin inflammation, anandamide (50 microg/50 microl) significantly reduced evoked neuronal responses, C-fibre mediated non-potentiated and post-discharge responses of neurones reduced to 65 +/- 5% and 57 +/- 10% of control, respectively. Effects of anandamide were blocked by SR141716A, a selective CB1 receptor antagonist. Spinal SR141716A (0.001-1 ng/50 microl) alone did not influence neuronal responses in inflamed rats. Spinal anandamide inhibited nociceptive transmission via CB1 receptors; following inflammation there is evidence for a loss of spinal endogenous cannabinoid tone.

摘要

内源性大麻素花生四烯乙醇胺对大麻素受体和香草酸受体具有亲和力,而这两种受体对伤害性感受传递具有相反的作用。本研究观察了鞘内注射花生四烯乙醇胺对非炎症状态和角叉菜胶致炎大鼠无害和有害刺激诱发的脊髓神经元反应的影响。花生四烯乙醇胺(0.1 - 50微克/50微升)对非炎症状态大鼠的作用并不一致。角叉菜胶致炎后,花生四烯乙醇胺(50微克/50微升)显著降低诱发的神经元反应,C纤维介导的神经元非增强反应和放电后反应分别降至对照的65±5%和57±10%。花生四烯乙醇胺的作用被选择性CB1受体拮抗剂SR141716A阻断。单独鞘内注射SR141716A(

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