Sagen J, Proudfit H K
Brain Res. 1981 Nov 2;223(2):391-6. doi: 10.1016/0006-8993(81)91153-7.
Previous studies have demonstrated that microinjection of noradrenergic (NA) antagonists such as phentolamine in the nucleus raphe magnus (NRM) produces hypoalgesia. This hypoalgesia appears to result from disinhibition of raphe-spinal serotonergic neurons since it is blocked by intrathecally injected methysergide. The present studies demonstrate that the hypoalgesia produced by microinjection of phentolamine in the NRM is also abolished by intrathecal administration of phentolamine. The results suggest that the hypoalgesia produced by microinjection of NA antagonists in the NRM is also mediated, at least in part, by the activation of spinally projecting NA neurons. Such hypoalgesia does not appear to be mediated by activation of enkephalinergic neurons since intrathecal injection of the opiate antagonist naloxone did not attenuate the hypoalgesia.
先前的研究表明,在中缝大核(NRM)微量注射去甲肾上腺素能(NA)拮抗剂如酚妥拉明会产生痛觉减退。这种痛觉减退似乎是由于中缝-脊髓5-羟色胺能神经元的去抑制作用所致,因为鞘内注射麦角新碱可阻断这种作用。目前的研究表明,鞘内注射酚妥拉明也可消除在NRM中微量注射酚妥拉明所产生的痛觉减退。结果提示,在NRM中微量注射NA拮抗剂所产生的痛觉减退至少部分也是由脊髓投射的NA神经元的激活所介导的。这种痛觉减退似乎不是由脑啡肽能神经元的激活所介导的,因为鞘内注射阿片拮抗剂纳洛酮并不能减弱痛觉减退。