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首页> 外文期刊>The European Journal of Neuroscience >Sympathetic activation triggers endogenous opioid release and analgesia within peripheral inflamed tissue.
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Sympathetic activation triggers endogenous opioid release and analgesia within peripheral inflamed tissue.

机译：交感神经激活触发周围发炎组织内源性阿片样物质释放和镇痛作用。

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摘要

Abstract Stress induces analgesia by mechanisms within and outside the brain. Here we show that the sympathetic nervous system is an essential trigger of intrinsic opioid analgesia within peripheral injured tissue. Noradrenaline, injected directly into inflamed hind paws of male Wistar rats, produced dose-dependent antinociception, reversible by alpha(1)-, alpha(2)- and beta(2)-antagonists. alpha(1)-, alpha(2)- and beta(2)-adrenergic receptors were demonstrated on beta-endorphin-containing immune cells and noradrenaline induced adrenergic receptor-specific release of beta-endorphin from immune cell suspensions. This antinociceptive effect of noradrenaline was reversed by micro - and delta-opioid antagonists as well as by anti-beta-endorphin. Stress-induced peripheral analgesia was abolished by chemical sympathectomy and by adrenergic antagonists. These findings indicate that sympathetic neuron-derived noradrenaline stimulates adrenergic receptors on inflammatory cells to release beta-endorphin, which induces analgesia via activation of peripheral opioid receptors.
机译：摘要压力通过大脑内部和外部的机制诱导镇痛作用。在这里，我们显示交感神经系统是周围受伤组织内发生阿片类镇痛的重要触发因素。将去甲肾上腺素直接注射到雄性Wistar大鼠发炎的后爪中，可产生剂量依赖性抗伤害感受，可被α（1）-，α（2）-和β（2）-拮抗剂逆转。在含β-内啡肽的免疫细胞上证实了α（1）-，α（2）-和β（2）-肾上腺素受体，而去甲肾上腺素诱导肾上腺素受体特异性从免疫细胞悬液中释放β-内啡肽。去甲肾上腺素的这种抗伤害感受作用被微和δ阿片类拮抗剂以及抗β-内啡肽逆转。化学交感神经切除术和肾上腺能拮抗剂消除了由压力引起的外周镇痛。这些发现表明，交感神经元衍生的去甲肾上腺素刺激炎性细胞上的肾上腺素能受体释放β-内啡肽，后者通过激活外周阿片受体来诱导镇痛作用。

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