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Proinflammatory signaling regulates voluntary alcohol intake and stress-induced consumption after exposure to social defeat stress in mice
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
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.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
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2017 (engelsk)Inngår i: Addiction Biology, ISSN 1355-6215, E-ISSN 1369-1600, Vol. 22, nr 5, s. 1279-1288Artikkel i tidsskrift (Fagfellevurdert) 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.

sted, utgiver, år, opplag, sider
John Wiley & Sons, 2017. Vol. 22, nr 5, s. 1279-1288
Emneord [en]
CPP; IL-1RI; TNF-1R; alcohol; cytokines; social defeat stress
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Identifikatorer
URN: urn:nbn:se:liu:diva-146330DOI: 10.1111/adb.12416ISI: 000408409700012PubMedID: 27273552OAI: oai:DiVA.org:liu-146330DiVA, id: diva2:1195947
Tilgjengelig fra: 2018-04-07 Laget: 2018-04-07 Sist oppdatert: 2024-01-10

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