Evidence map›Paper›PMID 26371763›Full record

ArticleTranslational psychiatry2015

Delayed emergence of behavioral and electrophysiological effects following juvenile ketamine exposure in mice.

L R Nagy, R E Featherstone, C G Hahn, S J Siegel

Abstract read
In one paragraph

Article in Translational psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
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  7. A roadmap for development of neuro-oscillations as translational biomarkers for treatment development in neuropsychopharmacology.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    Review
  8. Article
  9. Article
  10. Chronic administration of ketamine ameliorates the anxiety- and aggressive-like behavior in adolescent mice induced by neonatal maternal separation.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019
    Article
  11. Review
  12. Review
  13. Review
  14. Neurophysiological Characterization of Attentional Performance Dysfunction in Schizophrenia Patients in a Reverse-Translated Task.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
    Article
  15. Review
  16. Article
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.

L R NagyDepartment of Psychiatry, Translational Neuroscience Program, University of Pennsylvania, Philadelphia, PA, USA.
R E FeatherstoneDepartment of Psychiatry, Translational Neuroscience Program, University of Pennsylvania, Philadelphia, PA, USA.
C G HahnDepartment of Psychiatry, Translational Neuroscience Program, University of Pennsylvania, Philadelphia, PA, USA.
S J SiegelDepartment of Psychiatry, Translational Neuroscience Program, University of Pennsylvania, Philadelphia, PA, USA.

Funding

NMDA Receptor Hypofunction in the Amygdala of Schizophrenia PatientsP50MH096891 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI BILKER, WARREN B. · 2012 to 2016
$10.6M
Long-term neurobehavioral effects of ketamine exposure in adolescent miceR01DA023210 · NIDA · UNIVERSITY OF PENNSYLVANIA · PI SIEGEL, STEVEN J · 2008 to 2012
$1.9M
NIDA NIH HHS 5R01DA023210-02NIDA NIH HHS R01 DA023210NIMH NIH HHS 1-P50-MH-096891-02NIMH NIH HHS P50 MH096891
6 · The paper itself

Abstract

Frequent ketamine abuse in adulthood correlates with increased risk of psychosis, as well as cognitive deficits, including disruption of higher-order executive function and memory formation. Although the primary abusers of ketamine are adolescents and young adults, few studies have evaluated its effects on juvenile cognition. Therefore, the current study analyzes the effect of adolescent ketamine exposure on cognitive development. Juvenile mice (4 weeks of age) were exposed to chronic ketamine (20 mg kg(-1), i.p. daily) for 14 days. Mice were tested immediately after exposure in the juvenile period (7 weeks of age) and again as adults (12 weeks of age). Measures included electroencephalography (EEG) in response to auditory stimulation, the social choice test, and a 6-arm radial water maze task. Outcome measures include low-frequency EEG responses, event-related potential (ERP) amplitudes, indices of social behavior and indices of spatial working memory. Juvenile exposure to ketamine was associated with electrophysiological abnormalities in adulthood, particularly in induced theta power and the P80 ERP. The social choice test revealed that ketamine-exposed mice failed to exhibit the same age-related decrease in social interaction time as controls. Ketamine-exposed mice outperformed control mice as juveniles on the radial water maze task, but did not show the same age-related improvement as adult controls. These data support the hypothesis that juvenile exposure to ketamine produces long-lasting changes in brain function that are characterized by a failure to progress along normal developmental trajectories.

Indexed as

AnimalsBehavior, AnimalBrainCognitionCognition DisordersDisease Models, AnimalElectroencephalographyEvoked Potentials, AuditoryExcitatory Amino Acid AntagonistsKetamineMaleMemory, Short-TermMiceMice, Inbred C57BLReaction TimeTime FactorsExcitatory Amino Acid AntagonistsKetamine

Identifiers

PMID26371763
PMCPMC5068812

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Registered trials

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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.