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大麻类药物和大麻使用障碍引起的突触变化。

Synaptic changes induced by cannabinoid drugs and cannabis use disorder.

机构信息

Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, MD 20852, USA; Department of Pharmacology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.

Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, MD 20852, USA.

出版信息

Neurobiol Dis. 2022 Jun 1;167:105670. doi: 10.1016/j.nbd.2022.105670. Epub 2022 Feb 24.

DOI:10.1016/j.nbd.2022.105670
PMID:35219856
Abstract

The legalization of cannabis in many countries, as well as the decrease in perceived risks of cannabis, have contributed to the increase in cannabis use medicinally and recreationally. Like many drugs of abuse, cannabis and cannabis-derived drugs are prone to misuse, and long-term usage can lead to drug tolerance and the development of Cannabis Use Disorder (CUD). These drugs signal through cannabinoid receptors, which are expressed in brain regions involved in the neural processing of reward, habit formation, and cognition. Despite the widespread use of cannabis and cannabinoids as therapeutic agents, little is known about the neurobiological mechanisms associated with CUD and cannabinoid drug use. In this article, we discuss the advances in research spanning animal models to humans on cannabis and synthetic cannabinoid actions on synaptic transmission, highlighting the neurobiological mechanisms following acute and chronic drug exposure. This article also highlights the need for more research elucidating the neurobiological mechanisms associated with CUD and cannabinoid drug use.

摘要

在许多国家,大麻合法化以及对大麻风险认知的降低,导致大麻在医学和娱乐方面的使用增加。像许多滥用药物一样,大麻和大麻衍生药物容易被滥用,长期使用会导致药物耐受性和大麻使用障碍(CUD)的发展。这些药物通过大麻素受体发出信号,大麻素受体在涉及奖励、习惯形成和认知的大脑区域中表达。尽管大麻和大麻素被广泛用作治疗药物,但人们对与 CUD 和大麻素药物使用相关的神经生物学机制知之甚少。在本文中,我们讨论了从动物模型到人类的研究进展,这些研究涉及大麻和合成大麻素对突触传递的作用,重点介绍了急性和慢性药物暴露后的神经生物学机制。本文还强调了需要更多的研究来阐明与 CUD 和大麻素药物使用相关的神经生物学机制。

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