Making a bad thing worse: adverse effects of stress on drug addiction
Jessica N. Cleck, Julie A. Blendy
Jessica N. Cleck, Julie A. Blendy
Published February 1, 2008
Citation Information: J Clin Invest. 2008;118(2):454-461. https://doi.org/10.1172/JCI33946.
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Making a bad thing worse: adverse effects of stress on drug addiction

Abstract

Sustained exposure to various psychological stressors can exacerbate neuropsychiatric disorders, including drug addiction. Addiction is a chronic brain disease in which individuals cannot control their need for drugs, despite negative health and social consequences. The brains of addicted individuals are altered and respond very differently to stress than those of individuals who are not addicted. In this Review, we highlight some of the common effects of stress and drugs of abuse throughout the addiction cycle. We also discuss both animal and human studies that suggest treating the stress-related aspects of drug addiction is likely to be an important contributing factor to a long-lasting recovery from this disorder.

Authors

Jessica N. Cleck, Julie A. Blendy

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Figure 2

Reward and stress pathways in the brain.

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Reward and stress pathways in the brain. The mesolimbic dopamine reward ...
The mesolimbic dopamine reward pathway (blue) is composed of dopamine cell bodies in the VTA that project to the NAc. The VTA also projects to parts of the PFC and the amygdala (AMY). Central CRF circuitry (yellow) consists of CRF-containing cell bodies located in the central nucleus of the amygdala, which projects to the BNST. CRF projections from the amygdala also innervate the VTA, thus completing the circuit. The hypothalamic CRF projections are directed to the pituitary gland (PIT) located outside the blood-brain barrier. CRF in the pituitary gland stimulates the endocrine output of the HPA axis (red) including the release of ACTH, which acts on the adrenal gland to stimulate the secretion of cortisol in humans and corticosterone in rodents. A negative feedback system allows for cortisol-mediated regulation of continuous CRF production in the HPA axis.