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首页> 外文期刊>The European Journal of Neuroscience >Changes in endocannabinoid levels in a rat model of behavioural sensitization to morphine.
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Changes in endocannabinoid levels in a rat model of behavioural sensitization to morphine.

机译：对吗啡的行为敏感性大鼠模型中内源性大麻素水平的变化。

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Abstract The opioid and cannabinoid systems co-operate to regulate physiological processes such as nociception and reward. The endocannabinoid system may be a component of the brain reward circuitry and thus play a role not only in cannabinoid tolerance/dependence, but also in dependence/withdrawal for other misused drugs. We provide evidence of a cannabinoid mechanism in an animal model of morphine drug-seeking behaviour, referred to as behavioural sensitization. The present study was designed to test the effects of the CB(1) cannabinoid receptor antagonist SR141716A in two different phases of morphine sensitization (induction and expression) and to measure the brain contents of arachidonoylethanolamide (anandamide, AEA) and 2-arachidonoylglycerol (2-AG), the two main endogenous ligands for cannabinoid receptors in the different phases of morphine sensitization. The cannabinoid antagonist modified the signs of morphine sensitization when administered in the expression phase, whereas co-administration of SR141716A and morphine in the induction phase only slightly affected the behavioural responses, suggesting that CB(1) receptor blockade attenuates the behavioural manifestations of morphine sensitization but not its development. AEA and 2-AG were affected differently by morphine during the two phases of behavioural sensitization. The alterations were in opposite directions and specific for the cerebral area analysed (caudate putamen, nucleus accumbens, hippocampus and prefrontal cortex). The results suggest that the endocannabinoid system undergoes profound changes during the different phases of sensitization to morphine in rats, providing a possible neurochemical basis for the previously observed cross-sensitization between opiates and cannabinoids.
机译：摘要阿片和大麻素系统协同调节伤害和奖励等生理过程。内源性大麻素系统可能是大脑奖赏回路的组成部分，因此不仅在大麻素耐受性/依赖性方面，而且在对其他滥用药物的依赖性/退出方面都起着作用。我们提供了在吗啡药物寻求行为的动物模型中称为行为敏化的大麻素机制证据。本研究旨在测试CB（1）大麻素受体拮抗剂SR141716A在吗啡敏化的两个不同阶段（诱导和表达）的作用，并测量花生四烯酸乙醇酰胺（anandamide，AEA）和2-花生四烯酸甘油酯（2 -AG），这是吗啡敏化不同阶段中大麻素受体的两个主要内源性配体。在表达阶段给药时，大麻素拮抗剂会改变吗啡致敏的迹象，而在诱导阶段共同给药SR141716A和吗啡只会稍微影响行为反应，表明CB（1）受体阻滞减弱了吗啡致敏的行为表现但不是它的发展。在行为敏化的两个阶段中，吗啡对AEA和2-AG的影响不同。改变方向相反，并且针对所分析的大脑区域（尾状壳核，伏隔核，海马和前额叶皮层）。结果表明，在对吗啡致敏的不同阶段，内源性大麻素系统发生了深刻的变化，这为先前观察到的鸦片剂与大麻素之间的交叉致敏化提供了可能的神经化学基础。

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