Evidence map›Paper›PMID 35312993›Full record

ArticleCurrent topics in behavioral neurosciences2022

Ketamine for Depression: Advances in Clinical Treatment, Rapid Antidepressant Mechanisms of Action, and a Contrast with Serotonergic Psychedelics.

Marina Kojic, Johan Saelens, Bashkim Kadriu, Carlos A Zarate, Christoph Kraus

Open access · greenAbstract read
In one paragraph

Article in Current topics in behavioral neurosciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
15.3field-weighted citation impact, top 1% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. A novel psychedelic 5-HTJournal of psychopharmacology (Oxford, England) · 2026
    Trial
  3. Review
  4. Review
  5. Article
  6. 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

5 authors at 4 institutions in 2 countries.

Marina Kojic *Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria.
Johan Saelens *Department of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
Bashkim KadriuSection on the Neurobiology and Treatment of Mood Disorders, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA.
Carlos A ZarateSection on the Neurobiology and Treatment of Mood Disorders, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA.
Christoph KrausDepartment of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria. christoph.kraus@muv.ac.at.
Medical University of Vienna · ATJanssen (United States) · USNational Institute of Mental Health · USNational Institutes of Health · US

Funding

Glutamatergic Modulators for Rapid & Sustained Antidepressant EffectZIAMH002857 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI ZARATE, CARLOS · 2009 to 2025
$55.0M
Intramural NIH HHS ZIA MH002857
6 · The paper itself

Abstract

The approval of ketamine for treatment-resistant depression has created a model for a novel class of rapid-acting glutamatergic antidepressants. Recent research into other novel rapid-acting antidepressants - most notably serotonergic psychedelics (SPs) - has also proven promising. Presently, the mechanisms of action of these substances are under investigation to improve these novel treatments, which also exhibit considerable side effects such as dissociation. This chapter lays out the historical development of ketamine as an antidepressant, outlines its efficacy and safety profile, reviews the evidence for ketamine's molecular mechanism of action, and compares it to the proposed mechanism of SPs. The evidence suggests that although ketamine and SPs act on distinct primary targets, both may lead to rapid restoration of synaptic deficits and downstream network reconfiguration. In both classes of drugs, a glutamate surge activates α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) throughput and increases in brain-derived neurotrophic factor (BDNF) levels. Taken together, these novel antidepressant mechanisms may serve as a framework to explain the rapid and sustained antidepressant effects of ketamine and may be crucial for developing new rapid-acting antidepressants with an improved side effect profile.

Indexed as

HallucinogensKetamineAntidepressive AgentsDepressionReceptors, N-Methyl-D-AspartateAntidepressive AgentsHallucinogensKetamineReceptors, N-Methyl-D-AspartateAntidepressantsBrain-derived neurotrophic factorGlutamateSynaptic plasticityTreatment resistant depression

Identifiers

PMID35312993
PMCPMC10500612
OpenAlexW4220759286

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.