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首页> 外文期刊>The European Journal of Neuroscience >Reduction of stress-induced analgesia but not of exogenous opioid effects in mice lacking CB1 receptors.
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Reduction of stress-induced analgesia but not of exogenous opioid effects in mice lacking CB1 receptors.

机译：在缺乏CB1受体的小鼠中，减轻压力引起的镇痛作用，但不减轻外源性阿片类药物作用。

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摘要

CB1 cannabinoid receptors are widely distributed in the central nervous system where they mediate most of the cannabinoid-induced responses. Here we have evaluated the interactions between the CB1 cannabinoid receptors and the endogenous opioid system by assaying a number of well-characterized opioid responses, e.g. antinociception and stress-mediated effects, on mutant mice in which the CB1 receptor gene was invalidated. The spontaneous responses to various nociceptive stimuli (thermal, mechanical and visceral pain) were not changed in mutant CB1 mice. Furthermore, the absence of the CB1 cannabinoid receptor did not modify the antinociceptive effects induced by different opioid agonists: morphine (preferential mu opioid agonist), D-Pen2-D-Pen5-enkephalin (DPDPE) and deltorphin II (selective delta opioid agonists), and U-50,488H (selective kappa opioid agonist) in the hot-plate and tail-immersion tests. In contrast, the stress-induced opioid mediated responses were modified in CB1 mutants. Indeed, these mutants did not exhibit antinociception following a forced swim in water at 34 degrees C and presented a decrease in the immobility induced by the previous exposure to electric footshock. However, the antinociception induced by a forced swim in water at 10 degrees C was preserved in CB1 mutants. These results indicate that CB1 receptors are not involved in the antinociceptive responses to exogenous opioids, but that a physiological interaction between the opioid and cannabinoid systems is necessary to allow the development of opioid-mediated responses to stress.
机译：CB1大麻素受体广泛分布于中枢神经系统，它们介导大多数大麻素诱导的反应。在这里，我们通过分析许多特征明确的阿片类药物反应（例如，CB1大麻素受体和内源性阿片类药物系统）评估了CB1大麻素受体与内源性阿片类药物系统之间的相互作用。 CB1受体基因无效的突变小鼠的抗伤害感受和应激介导的作用。在突变CB1小鼠中，对各种伤害性刺激（热，机械和内脏痛）的自发反应没有改变。此外，不存在CB1大麻素受体并不能改变由不同的阿片类激动剂引起的镇痛作用：吗啡（首选mu阿片类激动剂），D-Pen2-D-Pen5-脑啡肽（DPDPE）和deltorphin II（选择性δ阿片类激动剂） ，以及在热板和尾部浸泡测试中使用U-50,488H（选择性Kappa阿片类激动剂）。相反，在CB1突变体中，应激诱导的阿片样物质介导的反应被修饰。确实，这些突变体在34°C的水中强迫游泳后并没有表现出抗伤害感受性，并且由于先前暴露于电休克中而引起的固定性降低。但是，在CB1突变体中保留了在10°C的水中强迫游泳诱导的抗伤害感受。这些结果表明，CB1受体不参与对外源阿片类药物的镇痛反应，但是阿片类药物和大麻素系统之间的生理相互作用对于允许产生阿片类药物介导的应激反应是必要的。

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