Evidence map›Paper›PMID 27226073›Full record

ArticleScientific reports2016

Prenatal ketamine exposure causes abnormal development of prefrontal cortex in rat.

Tianyun Zhao, Chuanxiang Li, Wei Wei, Haixing Zhang, Daqing Ma, Xingrong Song, Libing Zhou

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 58 citations in OpenAlex.

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  6. 15. Cluster Headache.Pain practice : the official journal of World Institute of Pain · 2025
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  17. Development of prefrontal cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
    Review
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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 4 institutions in 2 countries.

Tianyun ZhaoDepartment of Anesthesiology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, PR China.
Chuanxiang LiDepartment of Anesthesiology, Third Affiliated Hospital of Southern Medical University, Guangzhou, PR China.
Wei WeiDepartment of Anesthesiology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, PR China.
Haixing ZhangDepartment of Anesthesiology, Third Affiliated Hospital of Southern Medical University, Guangzhou, PR China.
Daqing MaAnaesthetics, Pain Medicine &Intensive Care, Department of Surgery &Cancer, Faculty of Medicine, Imperial College London, Chelsea and Westminster Hospital, London, UK.
Xingrong SongDepartment of Anesthesiology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, PR China.
Libing ZhouGuangdong-Hongkong-Macau Institute of CNS Regeneration, Ministry of Education CNS Regeneration Collaborative Joint Laboratory, Jinan University, Guangzhou, PR China.
Guangzhou Medical University · CNThird Affiliated Hospital of Southern Medical University · CNChelsea and Westminster Hospital · GBJinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ketamine is commonly used for anesthesia and as a recreational drug. In pregnant users, a potential neurotoxicity in offspring has been noted. Our previous work demonstrated that ketamine exposure of pregnant rats induces affective disorders and cognitive impairments in offspring. As the prefrontal cortex (PFC) is critically involved in emotional and cognitive processes, here we studied whether maternal ketamine exposure influences the development of the PFC in offspring. Pregnant rats on gestational day 14 were treated with ketamine at a sedative dose for 2 hrs, and pups were studied at postnatal day 0 (P0) or P30. We found that maternal ketamine exposure resulted in cell apoptosis and neuronal loss in fetal brain. Upon ketamine exposure in utero, PFC neurons at P30 showed more dendritic branching, while cultured neurons from P0 PFC extended shorter neurites than controls. In addition, maternal ketamine exposure postponed the switch of NR2B/2A expression, and perturbed pre- and postsynaptic protein expression in the PFC. These data suggest that prenatal ketamine exposure impairs neuronal development of the PFC, which may be associated with abnormal behavior in offsprings.

Indexed as

Prenatal Exposure Delayed EffectsAbnormalities, Drug-InducedAnesthetics, DissociativeAnimalsApoptosisBrainCells, CulturedDisks Large Homolog 4 ProteinExcitatory Amino Acid AntagonistsFemaleGestational AgeHypnotics and SedativesIllicit DrugsKetamineNeuritesNeuronsAnesthetics, DissociativeDisks Large Homolog 4 ProteinDlg4 protein, ratExcitatory Amino Acid AntagonistsHypnotics and SedativesIllicit DrugsKetamineNR2B NMDA receptorReceptors, N-Methyl-D-AspartateSynaptophysinSyp protein, rat

Identifiers

PMID27226073
PMCPMC4881038
OpenAlexW2398744811

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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.