A translational investigation targeting stress-reactivity and prefrontal cognitive control with guanfacine for smoking cessation
Open accessAbstract
Stress and prefrontal cognitive dysfunction have key roles in driving smoking; however, there are no therapeutics for smoking cessation that attenuate the effects of stress on smoking and enhance cognition. Central noradrenergic pathways are involved in stress-induced reinstatement to nicotine and in the prefrontal executive control of adaptive behaviors. We used a novel translational approach employing a validated laboratory analogue of stress-precipitated smoking, functional magnetic resonance imaging (fMRI), and a proof-of-concept treatment period to evaluate whether the noradrenergic α2a agonist guanfacine (3 mg/day) versus placebo (0 mg/day) reduced stress-precipitated smoking in the laboratory, altered cortico-striatal activation during the Stroop cognitive-control task, and reduced smoking following a quit attempt. In nicotine-deprived smokers ( n=33), stress versus a neutral condition significantly decreased the latency to smoke, and increased tobacco craving, ad-libitum smoking, and systolic blood pressure in placebo-treated subjects, and these effects were absent or reduced in guanfacine-treated subjects. Following stress, placebo-treated subjects demonstrated decreased cortisol levels whereas guanfacine-treated subjects demonstrated increased levels. Guanfacine, compared with placebo, altered prefrontal activity during a cognitive-control task, and reduced cigarette use but did not increase complete abstinence during treatment. These preliminary laboratory, neuroimaging, and clinical outcome data were consistent and complementary and support further development of guanfacine for smoking cessation.
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McKee et al. (2015) found guanfacine reduced stress-induced smoking in the lab and helped people quit smoking at home.
“McKee et al. (2015) found that guanfacine reduced stress-induced smoking in the lab, and helped people quit smoking at home.”
From Guanfacine’s mechanism of action in treating prefrontal cortical disorders: Successful translation across species (2020) · cites this paper as McKee et al. (2015)
The Discussion (page not supplied) reports that guanfacine reduced stress-precipitated smoking lapse in the laboratory and reduced cigarette use during a brief treatment period. It also says that an effect on complete abstinence was not demonstrated, so the claim that it helped people quit smoking at home overstates the finding. (LLM, conf=0.90)
Experimental — accuracy not yet measuredGuanfacine improves PFC functions and reduces cravings in subjects with stress-induced substance abuse.
“Guanfacine is now in widespread use for the treatment of PFC disorders on the basis of research in animals, and it has been shown to improve PFC functions and reduce cravings in subjects with stress-induced substance abuse112,113.”
From Stress weakens prefrontal networks: molecular insults to higher cognition (2015) · cites this paper as [112]
The Discussion reports reduced stress-related tobacco craving and increased prefrontal activity during a cognitive-control task in smokers receiving guanfacine. It interprets the neural findings as suggesting improved executive-control function, but reports no between-group difference in Stroop performance. The claim extends these findings in smokers to people with stress-induced substance abuse more broadly. (LLM, conf=0.85)
Experimental — accuracy not yet measured
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- Authors
- McKee, S. A., Potenza, M. N., Kober, H., Sofuoglu, M., Arnsten, A. F., Picciotto, M. R., Weinberger, A. H., Ashare, R., & Sinha, R.
- Affiliations
- Yale Cancer Center (US)
- Yale University (US)
- Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA
- University of Pennsylvania (US)
- ORCID
- Venue
- Journal of Psychopharmacology
- Publisher
- SAGE Publications
- Published
- 2014-12-16
- Volume
- 29
- Issue
- 3
- Pages
- 300-311
- ISSN
- 0269-8811 (ISSN-L)
- 1461-7285
- PMC
- PMC4376109
- OpenAlex
- W2018919329
- Cited by
- 75
- References
- 68
- Citations by year
- 2026: 2 · 2024: 3 · 2023: 3 · 2022: 6 · 2021: 4 · 2020: 8 · 2019: 11 · 2018: 11 · 2017: 9 · 2016: 8 · 2015: 10
- FWCI
- 6.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Psychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR000142)
- National Institute on Alcohol Abuse and Alcoholism (RL1AA017539)
- National Institute on Drug Abuse (R21DA033597, R01DA014241, RL1DA024857, P20DA027844, PL1DA024860, PL1DA024859, P50DA033945, K12DA000167, R37DA014241, R01DA035001)
- National Institute of Dental and Craniofacial Research (UL1DE019586)
- National Center for Research Resources (UL1RR024139)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Keywords
- guanfacine, smoking cessation, stress reactivity, nicotine craving, Stroop task, nicotine deprivation, cortisol, blood pressure
- MeSH terms
- Smoking Prevention, Adult, Blood Pressure, Cognition, Double-Blind Method, Humans, Hydrocortisone, Magnetic Resonance Imaging, Male, Middle Aged, Smoking, Stress, Psychological, Guanfacine, Smoking Cessation, Prefrontal Cortex, Young Adult, Adrenergic alpha-2 Receptor Agonists
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