Cannabis Addiction and the Brain: a Review

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Abstract

Cannabis is the most commonly used substance of abuse in the United States after alcohol and tobacco. With a recent increase in the rates of cannabis use disorder (CUD) and a decrease in the perceived risk of cannabis use, it is imperative to assess the addictive potential of cannabis. Here we evaluate cannabis use through the neurobiological model of addiction proposed by Koob and Volkow. The model proposes that repeated substance abuse drives neurobiological changes in the brain that can be separated into three distinct stages, each of which perpetuates the cycle of addiction. Here we review previous research on the acute and long-term effects of cannabis use on the brain and behavior, and find that the three-stage framework of addiction applies to CUD in a manner similar to other drugs of abuse, albeit with some slight differences. These findings highlight the urgent need to conduct research that elucidates specific neurobiological changes associated with CUD in humans.

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Drug addiction represents a dramatic dysregulation of motivational circuits that is caused by a combination of exaggerated incentive salience and habit formation, reward deficits and stress surfeits, and compromised executive function in three stages. The rewarding effects of drugs of abuse, development of incentive salience, and development of drug-seeking habits in the binge/intoxication stage involve changes in dopamine and opioid peptides in the basal ganglia. The increases in negative emotional states and dysphoric and stress-like responses in the withdrawal/negative affect stage involve decreases in the function of the dopamine component of the reward system and recruitment of brain stress neurotransmitters, such as corticotropin-releasing factor and dynorphin, in the neurocircuitry of the extended amygdala. The craving and deficits in executive function in the so-called preoccupation/anticipation stage involve the dysregulation of key afferent projections from the prefrontal cortex and insula, including glutamate, to the basal ganglia and extended amygdala. Molecular genetic studies have identified transduction and transcription factors that act in neurocircuitry associated with the development and maintenance of addiction that might mediate initial vulnerability, maintenance, and relapse associated with addiction.

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The conception of the ABCD study: From substance use to a broad NIH collaboration

Nora D. Volkow, George F Koob, Robert T Croyle … (2017)

Adolescence is a time of dramatic changes in brain structure and function, and the adolescent brain is highly susceptible to being altered by experiences like substance use. However, there is much we have yet to learn about how these experiences influence brain development, how they promote or interfere with later health outcomes, or even what healthy brain development looks like. A large longitudinal study beginning in early adolescence could help us understand the normal variability in adolescent brain and cognitive development and tease apart the many factors that influence it. Recent advances in neuroimaging, informatics, and genetics technologies have made it feasible to conduct a study of sufficient size and scope to answer many outstanding questions. At the same time, several Institutes across the NIH recognized the value of collaborating in such a project because of its ability to address the role of biological, environmental, and behavioral factors like gender, pubertal hormones, sports participation, and social/economic disparities on brain development as well as their association with the emergence and progression of substance use and mental illness including suicide risk. Thus, the Adolescent Brain Cognitive Development study was created to answer the most pressing public health questions of our day.

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Author and article information

Contributors

Gene-Jack Wang:

ORCID: http://orcid.org/0000-0002-5017-9905

gene-jack.wang@nih.gov

Journal

Journal ID (nlm-ta): J Neuroimmune Pharmacol

Journal ID (iso-abbrev): J Neuroimmune Pharmacol

Title: Journal of Neuroimmune Pharmacology

Publisher: Springer US (New York )

ISSN (Print): 1557-1890

ISSN (Electronic): 1557-1904

Publication date (Electronic): 19 March 2018

Publication date PMC-release: 19 March 2018

Publication date (Print): 2018

Volume: 13

Issue: 4

Pages: 438-452

Affiliations

[1 ]ISNI 0000 0004 0481 4802, GRID grid.420085.b, Laboratory of Neuroimaging, , National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, ; 10 Center Drive 31, Room B2L124, Bethesda, MD 20892 USA

[2 ]ISNI 0000 0004 0533 7147, GRID grid.420090.f, National Institute on Drug Abuse, National Institutes of Health, ; Bethesda, MD 20892 USA

Author information

Gene-Jack Wang http://orcid.org/0000-0002-5017-9905

Article

Publisher ID: 9782

DOI: 10.1007/s11481-018-9782-9

PMC ID: 6223748

PubMed ID: 29556883

SO-VID: 7926473c-9304-434f-b9f4-d3f8618c9478

License:

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.