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首页> 外文期刊>Life sciences >Opioid receptor upregulation in mu-opioid receptor deficient CXBK and outbred Swiss Webster mice.
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Opioid receptor upregulation in mu-opioid receptor deficient CXBK and outbred Swiss Webster mice.

机译：mu阿片受体缺乏的CXBK和近亲Swiss Webster小鼠中的阿片受体上调。

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摘要

Chronic in vivo treatment with opioid antagonists increases opioid receptor density and the potency of opioid agonists without altering receptor mRNA levels. To determine if basal receptor density affects opioid receptor upregulation, we examined the effect of chronic naltrexone treatment on mu-opioid receptor density and mRNA in two mice strains that differ in mu-opioid receptor density. CXBK mice (mu-opioid receptor deficient) and outbred Swiss Webster mice were implanted s.c. with a placebo or 15 mg naltrexone pellet for 8 days, the pellets removed and 24 hr later opioid receptor density (mu, delta) and receptor mRNA level (mu) determined in whole brain; or morphine dose-response studies conducted. In placebo-treated CXBK mice, mu-opioid receptor density was approximately 40% less than in Swiss Webster mice, although mu-opioid receptor mRNA abundance was similar in both strains. In placebo-treated CXBK mice, morphine potency was approximately 6-fold less than Swiss Webster mice. Naltrexone treatment increased morphine potency (1.7-fold) and mu- (approximately 90%) and delta- (approximately 20-40%) opioid receptor density in CXBK and Swiss Webster mouse brain similarly. Mu-opioid receptor mRNA was unchanged by naltrexone treatment in either strain. There was no difference in the basal or naltrexone-treated whole brain G(i alpha2) protein levels in CXBK or Swiss Webster mouse. These data indicate that a deficiency in mu-opioid receptors does not alter the regulation of opioid receptors by opioid antagonists in vivo, and suggest that adaptive responses to chronic opioid antagonist treatment are independent of opioid receptor density.
机译：阿片类拮抗剂的长期体内治疗可在不改变受体mRNA水平的情况下增加阿片类受体的密度和阿片激动剂的效力。为了确定基础受体密度是否影响阿片受体的上调，我们检查了慢性纳曲酮治疗对两种不同阿片受体浓度的小鼠品系中阿片受体浓度和mRNA的影响。将CXBK小鼠（μ阿片受体缺陷型）和近交Swiss Webster小鼠植入s.c.用安慰剂或15 mg纳曲酮沉淀8天，取出沉淀，并在24小时后确定全脑中的阿片样物质受体密度（μ，δ）和受体mRNA水平（μ）。或吗啡剂量反应研究。在安慰剂治疗的CXBK小鼠中，μ阿片受体的密度比Swiss Webster小鼠低约40％，尽管在两种菌株中μ阿片受体的mRNA丰度相似。在安慰剂治疗的CXBK小鼠中，吗啡效力比Swiss Webster小鼠低约6倍。纳曲酮治疗类似地增加了CXBK和Swiss Webster小鼠脑中的吗啡效价（1.7倍）和mu-（约90％）和del-（约20-40％）阿片受体密度。纳曲酮处理的任一菌株中，Mu类阿片受体mRNA均未改变。在CXBK或Swiss Webster小鼠中，基础或纳曲酮治疗的全脑G（i alpha2）蛋白水平没有差异。这些数据表明，μ阿片受体的缺乏不会改变阿片拮抗剂在体内对阿片受体的调节，并且表明对慢性阿片拮抗剂治疗的适应性反应与阿片受体密度无关。

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