Evidence map›Paper›PMID 27766766›Full record

ArticleAddiction biology2017

Region specific activation of the AKT and mTORC1 pathway in response to excessive alcohol intake in rodents.

Sophie Laguesse, Nadege Morisot, Khanhky Phamluong, Dorit Ron

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Addiction biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 40 citations in OpenAlex.

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  17. Protein Translation and Psychiatric Disorders.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2020
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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

4 authors at 1 institution in 1 country.

Sophie LaguesseDepartment of Neurology, University of California, San Francisco, USA.
Nadege MorisotDepartment of Neurology, University of California, San Francisco, USA.
Khanhky PhamluongDepartment of Neurology, University of California, San Francisco, USA.
Dorit RonDepartment of Neurology, University of California, San Francisco, USA.
University of California, San Francisco · US

Funding

Vector, Transgenic, and Imaging CoreP50AA017072 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RON, DORIT · 2008 to 2017
$13.9M
NIAAA NIH HHS P50 AA017072
6 · The paper itself

Abstract

We previously reported that the kinase AKT is activated in the nucleus accumbens (NAc) of rodents in response to excessive consumption of alcohol. One of the important downstream targets of AKT is the mammalian Target Of Rapamycin in Complex 1 (mTORC1), which was also activated by alcohol intake. mTORC1 controls dendritic protein translation, and we showed that the mTORC1-dependent translational machinery is activated in the NAc in response to alcohol intake. Importantly, systemic or intra-NAc inhibition of the AKT/mTORC1 pathway attenuated alcohol-drinking behaviors. Here, we mapped the activation patterns of AKT and mTORC1 in corticostriatal regions of rodents consuming large amounts of alcohol. We found that the activation of AKT and mTORC1 in response to cycles of binge drinking of 20 percent alcohol was centered in the NAc shell. Both kinases were not activated in the dorsolateral striatum (DLS); however, AKT, but not mTORC1, was activated in the dorsomedial striatum (DMS) of mice but not rats. Interestingly, excessive intake of alcohol produced a selective activation of the AKT/mTORC1 pathway in the orbitofrontal cortex (OFC), which was not observed in medial prefrontal cortex (mPFC). Furthermore, this signaling pathway was not activated in the NAc shell or OFC of rats consuming moderate amounts of alcohol nor was it activated in rats consuming sucrose. Together, our results suggest that excessive alcohol intake produces a brain region selective activation of the AKT/mTORC1 pathway, which is likely to contribute to NAc shell and OFC-dependent mechanisms that underlie the development and maintenance of alcohol drinking behavior.

Indexed as

AnimalsBehavior, AnimalBinge DrinkingBlotting, WesternBrainCentral Nervous System DepressantsDisease Models, AnimalEthanolMaleMechanistic Target of Rapamycin Complex 1Proto-Oncogene Proteins c-aktRatsRats, Long-EvansSignal TransductionCentral Nervous System DepressantsEthanolMechanistic Target of Rapamycin Complex 1Proto-Oncogene Proteins c-aktAKTAlcoholmTORC1

Identifiers

PMID27766766
PMCPMC5398951
OpenAlexW2535853985

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.