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Proinflammatory signaling regulates voluntary alcohol intake and stress-induced consumption after exposure to social defeat stress in mice
Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
Department of Physiology and Pharmacology, University of Georgia, Athens, GA.
Laboratory of Clinical and Translational Studies, National Institute of Alcohol Abuse and Alcoholism (NIAAA), National Institutes of Health (NIH), Bethesda, MD, USA.
Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
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2017 (English)In: Addiction Biology, ISSN 1355-6215, E-ISSN 1369-1600, Vol. 22, no 5, p. 1279-1288Article in journal (Refereed) Published
Abstract [en]

Proinflammatory activity has been postulated to play a role in addictive processes and stress responses, but the underlying mechanisms remain largely unknown. Here, we examined the role of interleukin 1 (IL-1) and tumor necrosis factor-a (TNF-a) in regulation of voluntary alcohol consumption, alcohol reward and stress-induced drinking. Mice with a deletion of the IL-1 receptor I gene (IL-1RI KO) exhibited modestly decreased alcohol consumption. However, IL-1RI deletion affected neither the rewarding properties of alcohol, measured by conditioned place preference (CPP), nor stress-induced drinking induced by social defeat stress. TNF-a signaling can compensate for phenotypic consequences of IL1-RI deletion. We therefore hypothesized that double deletion of both IL-1RI and TNF-1 receptors (TNF-1R) may reveal the role of these pathways in regulation of alcohol intake. Double KOs consumed significantly less alcohol than control mice over a range of alcohol concentrations. The combined deletion of TNF-1R and IL-1RI did not influence alcohol reward, but did prevent increased alcohol consumption resulting from exposure to repeated bouts of social defeat stress. Taken together, these data indicate that IL-1RI and TNF-1R contribute to regulation of stress-induced, negatively reinforced drinking perhaps through overlapping signaling events downstream of these receptors, while leaving rewarding properties of alcohol largely unaffected.

Place, publisher, year, edition, pages
John Wiley & Sons, 2017. Vol. 22, no 5, p. 1279-1288
Keywords [en]
CPP; IL-1RI; TNF-1R; alcohol; cytokines; social defeat stress
National Category
Substance Abuse
Identifiers
URN: urn:nbn:se:liu:diva-146330DOI: 10.1111/adb.12416ISI: 000408409700012PubMedID: 27273552OAI: oai:DiVA.org:liu-146330DiVA, id: diva2:1195947
Available from: 2018-04-07 Created: 2018-04-07 Last updated: 2018-04-07

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Karlsson, CamillaBjörk, KarlBarbier, EstelleEngblom, DavidThorsell, AnnikaHeilig, Markus

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Karlsson, CamillaStojakovic, AndreaBjörk, KarlBarbier, EstelleEngblom, DavidThorsell, AnnikaHeilig, Markus
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Center for Social and Affective NeuroscienceFaculty of Medicine and Health SciencesDivision of Cell BiologyDivision of Neuro and Inflammation ScienceDepartment of Psychiatry
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