Evidence map›Paper›PMID 28807788›Full record

ArticleNeuroscience2017

Adolescent binge ethanol exposure alters specific forebrain cholinergic cell populations and leads to selective functional deficits in the prefrontal cortex.

Gina M Fernandez, Lisa M Savage

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Ethanol inhibits dorsomedial striatum acetylcholine release.bioRxiv : the preprint server for biology · 2025
    Article
  5. Adolescent Alcohol and the Spectrum of Cognitive Dysfunction in Aging.Advances in experimental medicine and biology · 2025
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Gina M FernandezDepartment of Psychology, Behavioral Neuroscience Program, Binghamton University, State University of New York, USA.
Lisa M SavageDepartment of Psychology, Behavioral Neuroscience Program, Binghamton University, State University of New York, USA. Electronic address: lsavage@binghamton.edu.
Binghamton University · US

Funding

Cortical Biobehavioral Disruption after Thiamine Deficiency and Chronic AlcoholR01AA021775 · NIAAA · STATE UNIVERSITY OF NY,BINGHAMTON · PI SAVAGE, LISA M · 2014 to 2018
$2.3M
NIAAA NIH HHS R01 AA021775
6 · The paper itself

Abstract

Adolescence has been identified as a vulnerable developmental time period during which exposure to drugs can have long-lasting, detrimental effects. Although adolescent binge-like ethanol (EtOH) exposure leads to a significant reduction in forebrain cholinergic neurons, EtOH's functional effect on acetylcholine (ACh) release during behavior has yet to be examined. Using an adolescent intermittent ethanol exposure model (AIE), rats were exposed to binge-like levels of EtOH from postnatal days (PD) 25 to 55. Three weeks following the final EtOH exposure, cholinergic functioning was assessed during a spontaneous alternation protocol. During maze testing, ACh levels increased in both the hippocampus and prefrontal cortex. However, selectively in the prefrontal cortex, AIE rats displayed reduced levels of behaviorally relevant ACh efflux. We found no treatment differences in spatial exploration, spatial learning, spatial reversal, or novel object recognition. In contrast, AIE rats were impaired during the first attentional set shift on an operant set-shifting task, indicative of an EtOH-mediated deficit in cognitive flexibility. A unique pattern of cholinergic cell loss was observed in the basal forebrain following AIE: Within the medial septum/diagonal band there was a selective loss (30%) of choline acetyltransferase (ChAT)-positive neurons that were nestin negative (ChAT+/nestin-); whereas in the Nucleus basalis of Meynert (NbM) there was a selective reduction (50%) in ChAT+/nestin+. These results indicate that early adolescent binge EtOH exposure leads to a long-lasting frontocortical functional cholinergic deficit, driven by a loss of ChAT+/nestin+ neurons in the NbM, which was associated with impaired cognitive flexibility during adulthood.

Indexed as

AcetylcholineAgingAnimalsBasal ForebrainBasal Nucleus of MeynertCholine O-AcetyltransferaseCholinergic NeuronsEthanolHippocampusMalePrefrontal CortexProsencephalonRats, Sprague-DawleyAcetylcholineCholine O-AcetyltransferaseEthanol

Identifiers

PMID28807788
PMCPMC5609857
OpenAlexW2744486402

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.