Molecular and genetic substrates linking stress and addiction
Open accessAbstract
Drug addiction is one of the top three health concerns in the United States in terms of economic and health care costs. Despite this, there are very few effective treatment options available. Therefore, understanding the causes and molecular mechanisms underlying the transition from casual drug use to compulsive drug addiction could aid in the development of treatment options. Studies in humans and animal models indicate that stress can lead to both vulnerability to develop addiction, and increased drug taking and relapse in addicted individuals. Exposure to stress or drugs of abuse results in long-term adaptations in the brain that are likely to involve persistent alterations in gene expression or activation of transcription factors, such as the cAMP Response Element Binding (CREB) protein. The signaling pathways controlled by CREB have been strongly implicated in drug addiction and stress. Many potential CREB target genes have been identified based on the presence of a CRE element in promoter DNA sequences. These include, but are not limited to CRF, BDNF, and dynorphin. These genes have been associated with initiation or reinstatement of drug reward and are altered in one direction or the other following stress. While many reviews have examined the interactions between stress and addiction, the goal of this review was to focus on specific molecules that play key roles in both stress and addiction and are therefore posed to mediate the interaction between the two. Focus on these molecules could provide us with new targets for pharmacological treatments for addiction.
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Stressful experiences in early childhood make individuals more vulnerable to react intensively to stress in adolescents and adulthood and to develop mental disorders and addictive behaviors.
“Consistent with this notion, stressful experiences in early childhood make individuals more vulnerable to react intensively to stress in adolescents and adulthood (Elsey et al., 2015) and to develop mental disorders (Chen and Baram, 2016) and addictive behaviors (Briand and Blendy, 2010).”
From Integrating psychological and neurobiological considerations regarding the development and maintenance of specific Internet-use disorders: An Interaction of Person-Affect-Cognition-Execution (I-PACE) model (2016) · cites this paper as Briand and Blendy, 2010
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200 of 267 shown
- Authors
- Briand, L. A., & Blendy, J. A.
- Affiliations
- University of Pennsylvania (US)
- Corresponding author
- Blendy, Julie A.
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2010-02
- Volume
- 1314
- Pages
- 219-234
- ISSN
- 0006-8993 (ISSN-L)
- PMC
- PMC2819611
- OpenAlex
- W2032463884
- Cited by
- 125
- References
- 285
- Citations by year
- 2025: 2 · 2024: 4 · 2023: 4 · 2022: 9 · 2021: 8 · 2020: 6 · 2019: 6 · 2018: 5 · 2017: 6 · 2016: 11 · 2015: 5 · 2014: 9 · 2013: 12 · 2012: 18
- FWCI
- 1.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Drug Abuse (DA-11649)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- drug addiction, stress, CREB, CRF, brain-derived neurotrophic factor, dynorphin, drug relapse, drug reward, gene expression, addiction treatment targets
- MeSH terms
- Animals, Brain Chemistry, Corticotropin-Releasing Hormone, Dynorphins, Gene Expression Regulation, Humans, Neuronal Plasticity, Stress, Psychological, Cyclic AMP Response Element-Binding Protein, Brain-Derived Neurotrophic Factor, Substance-Related Disorders
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