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首页> 外文期刊>Neuron >Retention of supraspinal delta-like analgesia and loss of morphine tolerance in delta opioid receptor knockout mice.
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Retention of supraspinal delta-like analgesia and loss of morphine tolerance in delta opioid receptor knockout mice.

机译：在三角洲阿片受体敲除小鼠中保留棘上三角洲样镇痛和吗啡耐受性下降。

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Gene targeting was used to delete exon 2 of mouse DOR-1, which encodes the delta opioid receptor. Essentially all 3H-[D-Pen2,D-Pen5]enkephalin (3H-DPDPE) and 3H-[D-Ala2,D-Glu4]deltorphin (3H-deltorphin-2) binding is absent from mutant mice, demonstrating that DOR-1 encodes both delta1 and delta2 receptor subtypes. Homozygous mutant mice display markedly reduced spinal delta analgesia, but peptide delta agonists retain supraspinal analgesic potency that is only partially antagonized by naltrindole. Retained DPDPE analgesia is also demonstrated upon formalin testing, while the nonpeptide delta agonist BW373U69 exhibits enhanced activity in DOR-1 mutant mice. Together, these findings suggest the existence of a second delta-like analgesic system. Finally, DOR-1 mutant mice do not develop analgesic tolerance to morphine, genetically demonstrating a central role for DOR-1 in this process.
机译：基因靶向用于删除编码DΔ阿片受体的小鼠DOR-1的外显子2。基本上，突变小鼠不存在所有3H- [D-Pen2，D-Pen5]脑啡肽（3H-DPDPE）和3H- [D-Ala2，D-Glu4] deltorphin（3H-deltorphin-2）结合，表明DOR- 1编码delta1和delta2受体亚型。纯合突变小鼠表现出明显减少的脊髓三角镇痛作用，但肽三角洲激动剂保留了脊髓上镇痛作用，而纳曲酮仅能部分拮抗。福尔马林测试还证明了保留的DPDPE镇痛效果，而非肽δ激动剂BW373U69在DOR-1突变小鼠中表现出增强的活性。在一起，这些发现表明存在第二个类似三角洲的镇痛系统。最后，DOR-1突变小鼠对吗啡没有镇痛耐受性，从基因上证明了DOR-1在此过程中的重要作用。

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