Evidence map›Paper›PMID 26892295›Full record

ArticleNeuroscience2016

Developmental ethanol exposure-induced sleep fragmentation predicts adult cognitive impairment.

D A Wilson, K Masiello, M P Lewin, M Hui, J F Smiley, M Saito

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Impact of Developmental Alcohol Exposure on Sleep Physiology.Advances in experimental medicine and biology · 2025
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  20. Role of MCP-1 and CCR2 in alcohol neurotoxicity.Pharmacological research · 2019
    Review
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 2 institutions in 1 country.

D A WilsonDepartment of Child and Adolescent Psychiatry, NYU School of Medicine, New York, NY, United States; Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, United States. Electronic address: dwilson@nki.rfmh.org.
K MasielloNathan Kline Institute for Psychiatric Research, Orangeburg, NY, United States.
M P LewinDepartment of Child and Adolescent Psychiatry, NYU School of Medicine, New York, NY, United States; Sackler Neuroscience Graduate Program, NYU School of Medicine, New York, NY, United States.
M HuiNathan Kline Institute for Psychiatric Research, Orangeburg, NY, United States.
J F SmileyNathan Kline Institute for Psychiatric Research, Orangeburg, NY, United States; Department of Psychiatry, NYU School of Medicine, New York, NY, United States.
M SaitoNathan Kline Institute for Psychiatric Research, Orangeburg, NY, United States; Department of Psychiatry, NYU School of Medicine, New York, NY, United States.
Nathan Kline Institute for Psychiatric Research · USNew York University · US

Funding

Long-lasting consequences of early ethanol on network activity during sleepR01AA023181 · NIAAA · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI SAITO, MARIKO, SMILEY, JOHN F · 2014 to 2024
$3.6M
NIAAA NIH HHS R01 AA023181
6 · The paper itself

Abstract

Developmental ethanol (EtOH) exposure can lead to long-lasting cognitive impairment, hyperactivity, and emotional dysregulation among other problems. In healthy adults, sleep plays an important role in each of these behavioral manifestations. Here we explored circadian rhythms (activity, temperature) and slow-wave sleep (SWS) in adult mice that had received a single day of EtOH exposure on postnatal day 7 and saline littermate controls. We tested for correlations between slow-wave activity and both contextual fear conditioning and hyperactivity. Developmental EtOH resulted in adult hyperactivity within the home cage compared to controls but did not significantly modify circadian cycles in activity or temperature. It also resulted in reduced and fragmented SWS, including reduced slow-wave bout duration and increased slow-wave/fast-wave transitions over 24-h periods. In the same animals, developmental EtOH exposure also resulted in impaired contextual fear conditioning memory. The impairment in memory was significantly correlated with SWS fragmentation. Furthermore, EtOH-treated animals did not display a post-training modification in SWS which occurred in controls. In contrast to the memory impairment, sleep fragmentation was not correlated with the developmental EtOH-induced hyperactivity. Together these results suggest that disruption of SWS and its plasticity are a secondary contributor to a subset of developmental EtOH exposure's long-lasting consequences.

Indexed as

Alcohol-Related DisordersAnimalsBody TemperatureCentral Nervous System DepressantsCircadian RhythmCognitive DysfunctionConditioning, PsychologicalDisease Models, AnimalEthanolFearMemoryMice, Inbred C57BLMotor ActivityPrognosisSleepSleep DeprivationCentral Nervous System DepressantsEthanolcircadian rhythmfetal alcohol disorderinsomniasleep fragmentationslow-wave sleep

Identifiers

PMID26892295
PMCPMC4805438
OpenAlexW2287453840

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.