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Protein associated with addiction controls the oxycodone actions

机译:与成瘾相关的蛋白质控制羟考酮动作

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A key signaling protein in the brain known to play a critical role in the development of addiction-related behaviors acts as a positive modulator of oxycodone reward in both pain-free and chronic pain states, according to a study conducted at the Icahn School of Medicine at Mount Sinai and published online January 17 in the journal Neuropsychopharmacology. The mechanisms of oxycodone action uncovered through this study will help scientists and physicians develop strategies and tools to dissociate the analgesic (pain relief) actions of opioids from the addiction-related effects. Using mouse models of acute and chronic pain, Mount Sinai researchers found that RGS9-2, the intra-cellular protein that controls the function of opioid receptors in the brain reward center, promotes addiction to oxycodone in pain-free, acute, and chronic pain states. Mice that lacked the gene responsible for encoding RGS9-2 (RGS9KO mice) showed less propensity to develop addiction-related behaviors. Furthermore, the loss of RGS9-2 function does not affect the acute analgesic effects of oxycodone. The research team also found that RSG9-2 plays a protective role towards the development of oxycodone tolerance, as RGS9KO mice became tolerant to the analgesic effects of the drug earlier than those that had the gene. Researchers found that the same mechanisms control sensitivity to oxycodone addiction in pain-free as well as chronic pain states.
机译:根据ICAHN医学院进行的一项研究在西奈山,在线发表于1月17日的神经治科医生。通过本研究发现的羟考酮动作的机制将有助于科学家和医生制定策略和工具,以解散阿片类药物与成瘾相关的效果的镇痛(疼痛缓解)作用。使用急性和慢性疼痛的小鼠模型,山山研究人员发现RGS9-2,控制脑奖励中心在脑奖励中心中的阿片受体功能的细胞内蛋白质,促进无痛苦,急性和慢性疼痛对羟考酮的成瘾状态。缺乏负责编码RGS9-2(RGS9KO小鼠)的基因的小鼠表现出较少的发展成瘾相关行为的倾向。此外,RGS9-2功能的丧失不会影响羟考酮的急性镇痛作用。研究团队还发现RSG9-2对羟考酮耐受性发挥的保护作用,因为RGS9KO小鼠对药物早期的镇痛作用耐受性比具有基因的镇痛作用。研究人员发现,相同的机制控制对无痛苦和慢性疼痛状态的羟考酮成瘾的敏感性。

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