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首页> 外文期刊>The European Journal of Neuroscience >Lack of dependence and rewarding effects of deltorphin II in mu-opioid receptor-deficient mice.
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Lack of dependence and rewarding effects of deltorphin II in mu-opioid receptor-deficient mice.

机译：在阿片类鸦片受体缺陷型小鼠中缺乏deltorphin II的依赖性和奖励作用。

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摘要

We have previously shown that the antinociceptive effects produced by the delta opioid-selective agonist deltorphin II are preserved in mu-opioid receptor (MOR)-deficient mice. We have now investigated rewarding effects and physical dependence produced by deltorphin II in these animals. Wild-type and MOR-deficient mice were implanted with a cannula into the third ventricle and deltorphin II was administered centrally. The rewarding effects induced by deltorphin II were then investigated using the place preference paradigm. Wild-type mice showed place preference for the compartment previously associated with deltorphin II and this effect was not observed in MOR-deficient mice. In a second experiment, mice received a chronic perfusion of deltorphin II over 6 days, via an Alzet minipump connected to the intraventricular cannula, and withdrawal was precipitated by naloxone administration. Wild-type animals showed a moderate but significant incidence of several somatic signs of withdrawal. This withdrawal response was suppressed in MOR-deficient mice. Analysis of the immunoreactivity levels of PKC-alpha, PKC-beta (I and II) and PKC-gamma isozymes in the cerebral cortex of mice infused chronically with deltorphin II showed a significant up-regulation of all these isozymes in the soluble fraction in wild-type but not in MOR-deficient mice. In conclusion, mu-opioid receptors, which are not involved in deltorphin II antinociception, appear to mediate the effects of chronic deltorphin II on rewarding responses, physical dependence and adaptive changes to PKC.
机译：以前我们已经表明，在阿片类阿片受体（MOR）缺陷型小鼠中保留了由δ阿片类选择性激动剂deltorphin II产生的抗伤害作用。现在，我们研究了德尔托芬II对这些动物产生的有益作用和身体依赖性。将野生型和MOR缺陷型小鼠的套管植入第三脑室，并集中给予deltorphin II。然后，使用场所偏好范式研究了德尔托芬II诱导的奖励作用。野生型小鼠表现出对先前与deltorphin II相关的区室的位置偏好，并且在MOR缺陷小鼠中未观察到这种作用。在第二个实验中，小鼠通过连接到脑室内插管的Alzet微型泵在6天之内接受了deltorphin II的慢性灌注，并且通过纳洛酮的给药使撤离沉淀。野生型动物显示出中度但显着的几种躯体退缩迹象的发生率。在MOR缺陷小鼠中，这种戒断反应受到抑制。长期注射deltorphin II的小鼠大脑皮质中PKC-α，PKC-β（I和II）和PKC-γ同工酶的免疫反应性水平分析表明，野生环境中可溶性部分中的所有这些同工酶均显着上调-型，但不能出现在MOR缺陷型小鼠中。总之，不参与deltorphin II抗伤害感受的μ阿片受体似乎介导了慢性deltorphin II对PKC的奖励反应，身体依赖性和适应性改变的作用。

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