Evidence map›Paper›PMID 31819151›Full record

ArticleScientific reports2019

Chronic voluntary alcohol consumption causes persistent cognitive deficits and cortical cell loss in a rodent model.

Annai J Charlton, Carlos May, Sophia J Luikinga, Emma L Burrows, Jee Hyun Kim, Andrew J Lawrence, Christina J Perry

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 3 pooled it
32.1field-weighted citation impact, top 1% 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

22 citing papers in PubMed, 3 syntheses or guidelines pooled it, 313 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

7 authors at 2 institutions in 1 country.

Annai J CharltonFlorey Department of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, 3052, Australia.
Carlos MayFlorey Department of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, 3052, Australia.
Sophia J LuikingaMental Health Theme, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia.
Emma L BurrowsMental Health Theme, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia.
Jee Hyun KimMental Health Theme, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia.
Andrew J LawrenceMental Health Theme, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia.ORCID http://orcid.org/0000-0001-6836-727X
Christina J PerryMental Health Theme, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3052, Australia. christina.perry@florey.edu.au.ORCID http://orcid.org/0000-0002-6155-1469
The University of Melbourne · AUFlorey Institute of Neuroscience and Mental Health · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic alcohol use is associated with cognitive decline that impedes behavioral change during rehabilitation. Despite this, addiction therapy does not address cognitive deficits, and there is poor understanding regarding the mechanisms that underlie this decline. We established a rodent model of chronic voluntary alcohol use to measure ensuing cognitive effects and underlying pathology. Rats had intermittent access to alcohol or an isocaloric solution in their home cage under voluntary 2-bottle choice conditions. In Experiments 1 and 2 cognition was assessed using operant touchscreen chambers. We examined performance in a visual discrimination and reversal task (Experiment 1), and a 5-choice serial reaction time task (Experiment 2). For Experiment 3, rats were perfused immediately after cessation of alcohol access period, and volume, cell density and microglial populations were assessed in the prefrontal cortex and striatum. Volume was assessed using the Cavalieri probe, while cell and microglial counts were estimated using unbiased stereology with an optical fractionator. Alcohol-exposed and control rats showed comparable acquisition of pairwise discrimination; however, performance was impaired when contingencies were reversed indicating reduced behavioral flexibility. When tested in a 5-choice serial reaction time task alcohol-exposed rats showed increased compulsivity and increased attentional bias towards a reward associated cue. Consistent with these changes, we observed decreased cell density in the prefrontal cortex. These findings confirm a detrimental effect of chronic alcohol and establish a model of alcohol-induced cognitive decline following long-term voluntary intake that may be used for future intervention studies.

Indexed as

Alcohol DrinkingAlcoholismAnimalsCognitionCognitive DysfunctionDiscrimination LearningDisease Models, AnimalEthanolHumansPrefrontal CortexRatsReaction TimeEthanol

Identifiers

PMID31819151
PMCPMC6901469
OpenAlexW2996378856

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.