Evidence map›Paper›PMID 31135879›Full record

ArticleThe international journal of neuropsychopharmacology2019

Cognitive Impairment That Is Induced by (R)-Ketamine Is Abolished in NMDA GluN2D Receptor Subunit Knockout Mice.

Soichiro Ide, Yuiko Ikekubo, Masayoshi Mishina, Kenji Hashimoto, Kazutaka Ikeda

Open access · goldAbstract read
In one paragraph

Article in The international journal of neuropsychopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Negative allosteric modulation of α5-GABAbioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Potential Roles for the GluN2D NMDA Receptor Subunit in Schizophrenia.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. 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

5 authors at 3 institutions in 1 country.

Soichiro IdeAddictive Substance Project, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Yuiko IkekuboAddictive Substance Project, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Masayoshi MishinaAddictive Substance Project, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Kenji HashimotoCenter for Forensic Mental Health, Chiba University, Chuo-ku, Chiba, Japan.
Kazutaka IkedaAddictive Substance Project, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Tokyo Metropolitan Institute of Medical Science · JPCenter for Forensic Mental Health, Chiba University · JPRitsumeikan University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the N-methyl-D-aspartate receptor antagonist ketamine has attracted attention because of its rapid and sustained antidepressant effects in depressed patients, its side effects have raised some concerns. Ketamine is a racemic mixture of equal amounts of the enantiomers (R)-ketamine and (S)-ketamine. The neural mechanisms that underlie the differential effects of these enantiomers remain unclear. We investigated cognitive impairment that was induced by ketamine and its enantiomers in N-methyl-D-aspartate GluN2D receptor subunit knockout (GluN2D-KO) mice. In the novel object recognition test, (RS)-ketamine and (S)-ketamine caused cognitive impairment in both wild-type and GluN2D-KO mice, whereas (R)-ketamine induced such cognitive impairment only in wild-type mice. The present results suggest that the GluN2D subunit plays an important role in cognitive impairment that is induced by (R)-ketamine, whereas this subunit does not appear to be involved in cognitive impairment that is induced by (RS)-ketamine or (S)-ketamine.

Indexed as

AnimalsAntidepressive AgentsCognitive DysfunctionKetamineMice, Inbred C57BLMice, KnockoutReceptors, N-Methyl-D-AspartateRecognition, PsychologyAntidepressive AgentsKetamineNR2D NMDA receptorReceptors, N-Methyl-D-Aspartateantidepressantcognitive impairmentenantiomerGluN2Dketamine

Identifiers

PMID31135879
PMCPMC6600477
OpenAlexW2947558601

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.