Evidence map›Paper›PMID 21266194›Full record

ArticleBrain, behavior, and immunity2011

Activation of inflammatory signaling by lipopolysaccharide produces a prolonged increase of voluntary alcohol intake in mice.

Y A Blednov, J M Benavidez, C Geil, S Perra, H Morikawa, R A Harris

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

158 citing papers in PubMed, 1 synthesis or guideline pooled it, 241 citations in OpenAlex.

  1. Pooled it
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  4. Development of the Neuroimmune Modulator Ibudilast for the Treatment of Alcoholism: A Randomized, Placebo-Controlled, Human Laboratory Trial.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
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98 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Y A BlednovWaggoner Center for Alcohol and Addiction Research, University of Texas, 2500 Speedway MBB 1.124, Austin, TX 78712-0159, USA. yablednov@mail.utexas.edu
J M Benavidez
C Geil
S Perra
H Morikawa
R A Harris
The University of Texas at Austin · US

Funding

INIA: ANIMAL COREU01AA013520 · NIAAA · UNIVERSITY OF TEXAS AUSTIN · PI YURI A BLEDNOV, ROBERT O. MESSING · 2001 to 2026
$9.5M
BRAIN MEMBRANES IN ALCOHOL AND BENZODIAZEPINE DEPENDENCER01AA006399 · NIAAA · UNIVERSITY OF TEXAS AUSTIN · PI HARRIS, ROBERT A · 1985 to 2018
$8.8M
Alcohol Action on Neurons in the Brain Reward CircuitR01AA015521 · NIAAA · UNIVERSITY OF TEXAS AT AUSTIN · PI MORIKAWA, HITOSHI · 2007 to 2017
$2.4M
BRAIN MEMBRANES IN ALCOHOL AND BENZODIAZEPINE DEPENDENCER37AA006399 · NIAAA · UNIVERSITY OF TEXAS AUSTIN · PI HARRIS, ROBERT ADRON · 1989 to 1998
–
NIAAA NIH HHS AA015521NIAAA NIH HHS AA06399NIAAA NIH HHS AA U01 13520NIAAA NIH HHS R01 AA006399NIAAA NIH HHS R01 AA015521NIAAA NIH HHS R37 AA006399NIAAA NIH HHS U01 AA013520
6 · The paper itself

Abstract

Previous studies showed that mice with genetic predisposition for high alcohol consumption as well as human alcoholics show changes in brain expression of genes related to immune signaling. In addition, mutant mice lacking genes related to immune function show decreased alcohol consumption (Blednov et al., 2011), suggesting that immune signaling promotes alcohol consumption. To test the possibility that activation of immune signaling will increase alcohol consumption, we treated mice with lipopolysaccaride (LPS; 1mg/kg, i.p.) and tested alcohol consumption in the continuous two-bottle choice test. To take advantage of the long-lasting activation of brain immune signaling by LPS, we measured drinking beginning one week or one month after LPS treatment and continued the studies for several months. LPS produced persistent increases in alcohol consumption in C57BL/6J (B6) inbred mice, FVBxB6F1 and B6xNZBF1 hybrid mice, but not in FVB inbred mice. To determine if this effect of LPS is mediated through binding to TLR4, we tested mice lacking CD14, a key component of TLR4 signaling. These null mutants showed no increase of alcohol intake after treatment with LPS. LPS treatment decreased ethanol-conditioned taste aversion but did not alter ethanol-conditioned place preference (B6xNZBF1 mice). Electrophysiological studies of dopamine neurons in the ventral tegmental area showed that pretreatment of mice with LPS decreased the neuronal firing rate. These results suggest that activation of immune signaling promotes alcohol consumption and alters certain aspects of alcohol reward/aversion.

Indexed as

Alcohol DrinkingAnalysis of VarianceAnimalsChoice BehaviorConditioning, PsychologicalElectrophysiologyEthanolLipopolysaccharidesMiceNeuronsSelf AdministrationSpecies SpecificityEthanolLipopolysaccharides

Identifiers

PMID21266194
PMCPMC3098320
OpenAlexW2023256158

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.