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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Regulation of delta-opioid receptor trafficking via mu-opioid receptor stimulation: evidence from mu-opioid receptor knock-out mice.
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Regulation of delta-opioid receptor trafficking via mu-opioid receptor stimulation: evidence from mu-opioid receptor knock-out mice.

机译：通过μ阿片受体刺激调节δ阿片受体运输：从μ阿片受体敲除小鼠的证据。

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We recently demonstrated that prolonged treatment with morphine increases the antinociceptive potency of the delta-opioid receptor (deltaOR) agonist deltorphin and promotes cell surface targeting of deltaORs in neurons of the dorsal horn of the rat spinal cord (Cahill et al., 2001b). In the present study we examined whether these effects were mediated selectively via muOR. Using the same intermittent treatment regimen as for morphine, we found that methadone and etorphine, but not fentanyl, enhanced [D-Ala2]-deltorphin-mediated antinociception. However, continuous delivery of fentanyl for 48 hr resulted in augmented deltaOR-mediated antinociception when compared with saline-infused animals. Time course studies confirmed that a 48 hr treatment with morphine was necessary for the establishment of enhanced deltaOR-mediated antinociception. The observed increases in deltaOR agonist potency and deltaOR plasma membrane density were reversed fully 48 hr after discontinuation of morphine injections. Wild-type C57BL/6 mice pretreated with morphine for 48 hr similarly displayed enhanced deltaOR-mediated antinociception in a tonic pain paradigm. Accordingly, the percentage of plasma membrane-associated deltaOR in the dorsal horn of the spinal cord, as assessed by immunogold electron microscopy, increased from 6.6% in naive to 12.4% in morphine-treated mice. In contrast, morphine treatment of muOR gene knock-out (KO) mice did not produce any change in deltaOR plasma membrane density. These results demonstrate that selective activation of muOR is critical for morphine-induced targeting of deltaOR to neuronal membranes, but not for basal targeting of this receptor to the cell surface.
机译：我们最近证明了吗啡的长期治疗会增加δ-阿片受体（deltaOR）激动剂deltorphin的抗伤害感受力，并促进大鼠脊髓背角神经元中deltaORs的细胞表面靶向（Cahill et al。，2001b）。在本研究中，我们检查了这些效应是否通过muOR选择性介导。使用与吗啡相同的间歇治疗方案，我们发现美沙酮和依托啡但非芬太尼可增强[D-Ala2] -deltorphin介导的镇痛作用。但是，与注入盐水的动物相比，连续芬太尼连续递送48小时会导致deltaOR介导的抗伤害感受增强。时程研究证实，建立增强的deltaOR介导的抗伤害感受必须用吗啡治疗48小时。停用吗啡后48小时，观察到的delOR激动剂效力和delOR质膜密度的增加被完全逆转。用吗啡预处理48小时的野生型C57BL / 6小鼠在强直性疼痛范例中同样表现出增强的deltaOR介导的抗伤害感受。因此，通过免疫金电子显微镜评估，脊髓背角中与质膜相关的deltaOR的百分比从幼稚期的6.6％增加到吗啡处理的小鼠的12.4％。相比之下，对吗啡基因敲除（KO）小鼠进行吗啡治疗并未使delOROR质膜密度产生任何变化。这些结果表明，muOR的选择性激活对于吗啡诱导的deltaOR对神经元膜的靶向作用至关重要，但对于该受体对细胞表面的基础靶向作用则不是关键。

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