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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Antisense oligodeoxynucleotides to the kappa1 receptor enhance delta9-THC-induced antinociceptive tolerance.
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Antisense oligodeoxynucleotides to the kappa1 receptor enhance delta9-THC-induced antinociceptive tolerance.

机译：对kappa1受体的反义寡聚脱氧核苷酸增强了delta9-THC诱导的抗伤害感受性。

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摘要

Delta-9-tetrahydrocannabinol produces potent antinociceptive effects in mice and rats. Evidence exists for an interaction between the cannabinoids and the kappa receptor subtype, kappa1, in the production of antinociception. Data indicate that delta9-THC induces the release of endogenous dynorphins, the ligand(s) for the kappa receptor. It has been demonstrated that antisense oligodeoxynucleotides directed against the kappa1 receptor attenuate the antinociceptive effects of delta9-THC. The exact mechanism for the expression of cannabinoid tolerance is unknown. Bidirectional cross-tolerance between the kappa opioids and delta9-THC implies that a common mechanism may be responsible for tolerance expression. We tested the hypothesis that the kappa1 receptor is involved in tolerance to delta9-THC. Antisense to the kappa1 receptor has been shown to downregulate the kappa receptor. We observed a significant increase in the ED50 for delta9-THC in antisense-, but not mismatch-treated mice, indicating an increase in tolerance to delta9-THC. Such data indicate that a decrease in kappa receptor number may accompany tolerance to delta9-THC.
机译：Delta-9-四氢大麻酚可在小鼠和大鼠中产生有效的镇痛作用。有证据表明，在产生抗伤害感受的过程中，大麻素与kappa受体亚型kappa1之间存在相互作用。数据表明，delta9-THC诱导释放内源性强啡肽，即κ受体的配体。已经证明，针对kappa1受体的反义寡脱氧核苷酸减弱了delta9-THC的抗伤害感受作用。表达大麻素耐受性的确切机制尚不清楚。 Kappa阿片类药物和delta9-THC之间的双向交叉耐受性意味着共同的机制可能负责耐受性表达。我们检验了kappa1受体参与delta9-THC耐受性的假设。业已证明，对kappa1受体的反义作用可下调kappa受体。我们观察到在反义处理但未错配处理的小鼠中，delta9-THC的ED50显着增加，表明对delta9-THC的耐受性增加。这样的数据表明，κ受体数目的减少可能伴随对delta9-THC的耐受性。

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