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Proinflammatory signaling regulates voluntary alcohol intake and stress-induced consumption after exposure to social defeat stress in mice

Overview of attention for article published in Addiction Biology, June 2016
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3 tweeters
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1 Facebook page

Citations

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8 Dimensions

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24 Mendeley
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Title
Proinflammatory signaling regulates voluntary alcohol intake and stress-induced consumption after exposure to social defeat stress in mice
Published in
Addiction Biology, June 2016
DOI 10.1111/adb.12416
Pubmed ID
Authors

Karlsson, Camilla, Schank, Jesse R., Rehman, Faazal, Stojakovic, Andrea, Björk, Karl, Barbier, Estelle, Solomon, Matthew, Tapocik, Jenica, Engblom, David, Thorsell, Annika, Heilig, Markus, Schank, Jesse R, Camilla Karlsson, Jesse R. Schank, Faazal Rehman, Andrea Stojakovic, Karl Björk, Estelle Barbier, Matthew Solomon, Jenica Tapocik, David Engblom, Annika Thorsell, Markus Heilig

Abstract

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-α (TNF-α) 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-α 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.

Twitter Demographics

The data shown below were collected from the profiles of 3 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 24 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 4%
Unknown 23 96%

Demographic breakdown

Readers by professional status Count As %
Student > Master 6 25%
Student > Bachelor 6 25%
Student > Ph. D. Student 3 13%
Student > Doctoral Student 3 13%
Researcher 2 8%
Other 4 17%
Readers by discipline Count As %
Neuroscience 6 25%
Agricultural and Biological Sciences 3 13%
Biochemistry, Genetics and Molecular Biology 3 13%
Social Sciences 2 8%
Psychology 2 8%
Other 8 33%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 17 May 2018.
All research outputs
#7,283,663
of 12,134,677 outputs
Outputs from Addiction Biology
#450
of 692 outputs
Outputs of similar age
#139,955
of 277,100 outputs
Outputs of similar age from Addiction Biology
#6
of 11 outputs
Altmetric has tracked 12,134,677 research outputs across all sources so far. This one is in the 37th percentile – i.e., 37% of other outputs scored the same or lower than it.
So far Altmetric has tracked 692 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 9.4. This one is in the 32nd percentile – i.e., 32% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 277,100 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 45th percentile – i.e., 45% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 11 others from the same source and published within six weeks on either side of this one. This one is in the 45th percentile – i.e., 45% of its contemporaries scored the same or lower than it.