内源性和外源性阿片类物质:在药物使用障碍中的作用。

Q3 Neuroscience Advances in neurobiology Pub Date : 2024-01-01 DOI:10.1007/978-3-031-45493-6_14
Lindsay Acree
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引用次数: 0

摘要

近年来,阿片类药物使用障碍已成为一种流行病,根据美国疾病控制和预防中心(Centers for Disease Control, Wide Rangeing Online Data for epidemiologic research (WONDER))的数据,自 1999 年以来,阿片类药物使用障碍的发病率几乎翻了两番。美国疾病预防控制中心,国家卫生统计中心,亚特兰大。2017年12月19日,从http://wonder.cdc.gov,2016年)。要将药物使用障碍(SUD)理解为一种疾病,必须对许多方面进行研究,包括大脑回路、神经元回路和神经递质的适应性、增加 SUD 风险的基因变异以及可用于 SUD 的治疗方法。外源性阿片类药物可能导致药物依赖性成瘾的机制与内源性阿片类药物的机制几乎相同。本章回顾了阿片类药物使用障碍的临床和流行病学方面,以及内源性和外源性阿片类药物之间的相互作用。此外,本章还讨论了当前有关遗传变异和大脑回路机制的科学数据,以及内源性阿片类药物在一般药物使用障碍(特别是阿片类药物使用障碍)中的作用。本章还讨论了这些数据在药物使用障碍治疗中的未来应用。
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Endogenous and Exogenous Opioids: Role in Substance Use Disorders.

Opioid use disorders have become an epidemic in recent years with rates nearly quadrupling since 1999 according to the US Centers for Disease Control and Prevention (Centers for Disease Control, Wide-ranging online data for epidemiologic research (WONDER). CDC, National Center for Health Statistics, Atlanta. Retrieved December 19, 2017, from http://wonder.cdc.gov, 2016). To understand substance use disorder (SUD) as a disease, many aspects must be studied including the circuitry in the brain, adaptations to neuronal circuitry and neurotransmitters, genetic variations increasing the risk for SUD, and treatments available for SUD. The mechanism in which an exogenous opioid may cause SUD is nearly identical to the mechanism of an endogenous opioid. This chapter reviews the clinical and epidemiological aspects of opioid use disorder, as well as the interactions between endogenous and exogenous opioids. Additionally, this chapter discusses current scientific data regarding genetic variations and mechanisms within brain circuitry and the role of endogenous opioids in substance use disorders generally (and opioid use disorder specifically). Future applications of these data to treatment of substance use disorders are also discussed.

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来源期刊
Advances in neurobiology
Advances in neurobiology Neuroscience-Neurology
CiteScore
2.80
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0
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