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Neurological correlates of brain reward circuitry linked to opioid use disorder (OUD): Do homo sapiens acquire or have a reward deficiency syndrome?
Journal of the Neurological Sciences ( IF 3.6 ) Pub Date : 2020-11-01 , DOI: 10.1016/j.jns.2020.117137
Mark S Gold 1 , David Baron 2 , Abdalla Bowirrat 3 , Kenneth Blum 2
Affiliation  

The extant literature confirms that an array of polymorphic genes related to- neurotransmitters and second messengers govern the net release of dopamine in the Nucleus Accumbens (NAc) in the mesolimbic region of the brain. They are linked predominantly to motivation, anti-stress, incentive salience (wanting), and wellbeing. Notably, in 2000 the Nobel Prize was awarded to Carlsson, Greengard, and Kandel for their work on the molecular and cellular function of dopaminergic activity at neurons. This historical psychopharmacological work involved neurotransmission of serotonin, endorphins, glutamate, and dopamine, and the seminal work of Blum, Gold, Volkow, Nestler, and others related to neurotransmitter function and related behaviors. Currently, Americans are facing their second and worst opioid epidemic, prescribed opioids, and easy access drive this epidemic of overdoses, and opioid use disorders (OUDs). Presently the clinical consensus is to treat OUD, as if it were an opioid deficiency syndrome, with long-term to life-long opioid substitution therapy. Opioid agonist administration is seen as necessary to replace missing opioids, treat OUD, and prevent overdoses, like insulin is used to treat diabetes. Treatment of OUD and addiction, in general, is similar to the endocrinopathy conceptualization in that it views opioid agonist MATs as an essential core to therapy. Is this approach logical? Other than as harm reduction, is using opioids to treat OUD therapeutic or harmful in the long term? This historical Trieste provides a molecular framework to understand the current underpinnings of endorphinergic/dopaminergic mechanisms related to opioid deficiency syndrome and generalized reward processing depletion. WC 249.

中文翻译:

与阿片类药物使用障碍 (OUD) 相关的大脑奖赏回路的神经学相关性:智人是否获得或患有奖赏缺乏综合症?

现有文献证实,一系列与神经递质和第二信使相关的多态性基因控制着大脑中脑边缘区伏隔核 (NAc) 中多巴胺的净释放。它们主要与动机、抗压力、激励显着性(想要)和幸福感有关。值得注意的是,2000 年诺贝尔奖授予 Carlsson、Greengard 和 Kandel,以表彰他们在神经元多巴胺能活动的分子和细胞功能方面的工作。这项历史性的精神药理学工作涉及血清素、内啡肽、谷氨酸盐和多巴胺的神经传递,以及 Blum、Gold、Volkow、Nestler 和其他与神经递质功能和相关行为相关的开创性工作。目前,美国人正面临第二次也是最严重的阿片类药物流行病 和易于获取推动了这种过量服用和阿片类药物使用障碍 (OUD) 的流行。目前临床上的共识是将 OUD 视为阿片类药物缺乏综合征,采用长期至终生的阿片类药物替代疗法。阿片类激动剂被认为是替代缺失的阿片类药物、治疗 OUD 和预防过量服用的必要手段,就像胰岛素用于治疗糖尿病一样。总体而言,对 OUD 和成瘾的治疗类似于内分泌病的概念化,因为它将阿片受体激动剂 MAT 视为治疗的基本核心。这种方法合乎逻辑吗?除了减少伤害,从长远来看,使用阿片类药物治疗 OUD 是治疗性的还是有害的?这一历史的里雅斯特提供了一个分子框架,以了解与阿片类药物缺乏综合征和广义奖励处理耗竭相关的内啡肽/多巴胺能机制的当前基础。厕所 249。
更新日期:2020-11-01
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