Evidence map›Paper›PMID 27934938›Full record

ArticleScientific reports2016

Changes in hippocampal AMPA receptors and cognitive impairments in chronic ketamine addiction models: another understanding of ketamine CNS toxicity.

Runtao Ding, Yanning Li, Ao Du, Hao Yu, Bolin He, Ruipeng Shen, Jichuan Zhou, Lu Li, Wen Cui, Guohua Zhang and 2 more

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 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
1.2field-weighted citation impact, top 25% 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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 80 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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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

12 authors at 2 institutions in 1 country.

Runtao DingDepartment of Forensic Pathology, School of Forensic Medicine, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, P. R. China.
Yanning LiDepartment of Forensic Pathology, School of Forensic Medicine, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, P. R. China.
Ao DuDepartment of Forensic Pathology, School of Forensic Medicine, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, P. R. China.
Hao YuDepartment of Forensic Pathology, School of Forensic Medicine, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, P. R. China.
Bolin HeDepartment of Forensic Pathology, School of Forensic Medicine, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, P. R. China.
Ruipeng ShenDepartment of Forensic Pathology, School of Forensic Medicine, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, P. R. China.
Jichuan ZhouKey Laboratory of Health Ministry in Congenital Malformation, the Affiliated Shengjing Hospital of China Medical University, Shenyang 110004, P. R. China.
Lu LiDepartment of Forensic and Medical Laboratory, Jining Medical University, 16 Hehua Road, Jining 272067, P. R. China.
Wen CuiDepartment of Forensic and Medical Laboratory, Jining Medical University, 16 Hehua Road, Jining 272067, P. R. China.
Guohua ZhangDepartment of Forensic Pathology, School of Forensic Medicine, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, P. R. China.
Yan LuKey Laboratory of Health Ministry in Congenital Malformation, the Affiliated Shengjing Hospital of China Medical University, Shenyang 110004, P. R. China.
Xu WuDepartment of Forensic Pathology, School of Forensic Medicine, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang 110122, P. R. China.
China Medical University · CNJining Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ketamine has been reported to impair human cognitive function as a recreational drug of abuse. However, chronic effects of ketamine on central nervous system need to be further explored. We set out to establish chronic ketamine addiction models by giving mice a three or six month course of daily intraperitoneal injections of ketamine, then examined whether long-term ketamine administration induced cognition deficits and changed hippocampal post-synaptic protein expression in adult mice. Behavior tests results showed that mice exhibited dose- and time-dependent learning and memory deficits after long-term ketamine administration. Western blot results showed levels of GluA1, p-S845 and p-S831 proteins demonstrated significant decline with ketamine 60 mg/kg until six months administration paradigm. But levels of p-S845 and p-S831 proteins exhibited obvious increase with ketamine 60 mg/kg three months administration paradigm. NR1 protein levels significantly decrease with ketamine 60 mg/kg three and six months administration paradigm. Our results indicate that reduced expression levels and decreased phosphorylation levels of hippocampal post-synaptic membrane GluA1- containing AMPA receptors maybe involved in cognition impairment after long-term ketamine administration. These findings provide further evidence for the cognitive damage of chronic ketamine addiction as a recreational drug.

Indexed as

Models, BiologicalAnimalsCentral Nervous SystemCognition DisordersDose-Response Relationship, DrugHippocampusKetamineMiceNerve Tissue ProteinsReceptors, AMPASubstance-Related DisordersKetamineNerve Tissue ProteinsReceptors, AMPA

Identifiers

PMID27934938
PMCPMC5146946
OpenAlexW2560822022

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.