Herz A, Millan M
Farmakol Toksikol. 1989 May-Jun;52(3):5-12.
At the cerebral level, studies employing several experimental approaches point to an essential role of beta-endorphin in analgesia, induced by electrical stimulation of the periaqueductal grey of the midbrain. Tolerance and cross-tolerance studies suggest that mu-opioid receptors mediate this effect. The significance of sigma- and, in particular, kappa-opioid receptors in cerebral pain modulation is less well documented. At the spinal level, nociception is relayed in the dorsal horn, where opioid peptides as well as all types of opioid receptors are abundant. mu-opioid receptor-mediated anti-nociceptive processes appear to be most important in this region, but sigma-opioid receptors may also be involved. In addition, a role of kappa-opioid receptors can be demonstrated under certain conditions. Recent experiments indicate that opioids may also modulate nociception in the periphery, in particular in inflamed tissue.
在大脑层面,采用多种实验方法的研究表明,β-内啡肽在中脑导水管周围灰质电刺激诱导的镇痛中起关键作用。耐受性和交叉耐受性研究表明,μ-阿片受体介导了这种效应。关于σ-阿片受体,尤其是κ-阿片受体在大脑疼痛调节中的意义,文献记载较少。在脊髓层面,伤害性刺激在背角传导,背角富含阿片肽以及所有类型的阿片受体。μ-阿片受体介导的抗伤害感受过程在该区域似乎最为重要,但σ-阿片受体也可能参与其中。此外,在某些条件下可以证明κ-阿片受体的作用。最近的实验表明,阿片类药物也可能在外周,特别是在炎症组织中调节伤害性感受。