Evidence map›Paper›PMID 25446758›Full record

ArticleBehavioural brain research2015

Traumatic brain injury induces neuroinflammation and neuronal degeneration that is associated with escalated alcohol self-administration in rats.

Jacques P Mayeux, Sophie X Teng, Paige S Katz, Nicholas W Gilpin, Patricia E Molina

Abstract read
In one paragraph

Article in Behavioural brain research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

47 citing papers in PubMed, 74 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Jacques P MayeuxDepartment of Physiology and Alcohol and Drug Abuse Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, LA 70112, United States.
Sophie X TengDepartment of Physiology and Alcohol and Drug Abuse Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, LA 70112, United States.
Paige S KatzDepartment of Physiology and Alcohol and Drug Abuse Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, LA 70112, United States.
Nicholas W GilpinDepartment of Physiology and Alcohol and Drug Abuse Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, LA 70112, United States.
Patricia E MolinaDepartment of Physiology and Alcohol and Drug Abuse Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, LA 70112, United States. Electronic address: pmolin@lsuhsc.edu.
Louisiana State University Health Sciences Center New Orleans · US

Funding

BIOMEDICAL ALCOHOL RESEARCH TRAINING PROGRAMT32AA007577 · NIAAA · LSU HEALTH SCIENCES CENTER · PI PATRICIA E. MOLINA · 1999 to 2026
$9.6M
Brain Injury and Alcohol: Neuropathological Mechanisms of Impaired RecoveryF30AA022838 · NIAAA · LSU HEALTH SCIENCES CENTER · PI TENG, SOPHIE XU · 2013 to 2015
$115k
NIAAA NIH HHS F30 AA022838NIAAA NIH HHS T-32 AA007577NIAAA NIH HHS T32 AA007577
6 · The paper itself

Abstract

backgroundTraumatic brain injury (TBI) affects millions of people each year and is characterized by direct tissue injury followed by a neuroinflammatory response. The post-TBI recovery period can be associated with a negative emotional state characterized by alterations in affective behaviors implicated in the development of Alcohol Use Disorder in humans. The aim of this study was to test the hypothesis that post-TBI neuroinflammation is associated with behavioral dysfunction, including escalated alcohol intake.

methodsAdult male Wistar rats were trained to self-administer alcohol prior to counterbalanced assignment into naïve, craniotomy, and TBI groups by baseline drinking. TBI was produced by lateral fluid percussion (LFP; >2 ATM; 25ms). Alcohol drinking and neurobehavioral function were measured at baseline and following TBI in all experimental groups. Markers of neuroinflammation (GFAP and ED1) and neurodegeneration (FJC) were determined by fluorescence histochemistry in brains excised at sacrifice 19 days post-TBI.

resultsThe cumulative increase in alcohol intake over the 15 days post-TBI was greater in TBI animals compared to naïve controls. A higher rate of pre-injury alcohol intake was associated with a greater increase in post-injury alcohol intake in both TBI and craniotomy animals. Immediately following TBI, both TBI and craniotomy animals exhibited greater neurobehavioral dysfunction compared to naïve animals. GFAP, IBA-1, ED1, and FJC immunoreactivity at 19 days post-TBI was significantly higher in brains from TBI animals compared to both craniotomy and naïve animals.

conclusionsThese results show an association between post-TBI escalation of alcohol drinking and marked localized neuroinflammation at the site of injury. Moreover, these results highlight the relevance of baseline alcohol preference in determining post-TBI alcohol drinking. Further investigation to determine the contribution of neuroinflammation to increased alcohol drinking post-TBI is warranted.

Indexed as

Alcohol DrinkingAnimalsBrain InjuriesEncephalitisEthanolMaleNeuronsRatsRats, WistarSelf AdministrationEthanolAlcoholAnxietyNeuroinflammationSelf-administrationTraumatic brain injury

Identifiers

PMID25446758
PMCPMC4277916
OpenAlexW2031479223

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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.