Evidence map›Paper›PMID 31830487›Full record

ReviewPharmacology, biochemistry, and behavior2020

Neurotrophic mechanisms underlying the rapid and sustained antidepressant actions of ketamine.

Satoshi Deyama, Ronald S Duman

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology, biochemistry, and behavior, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 3 pooled it
15.8field-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

81 citing papers in PubMed, 3 syntheses or guidelines pooled it, 178 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Review
  7. Article
  8. Review
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  11. Article
  12. Ketamine Reverses Chronic Stress-Induced Behavioral Changes via the Expression of CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  13. Article
  14. Chronic, combinatorial targeting of NMDARs and 5-HTNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

21 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Satoshi DeyamaLaboratory of Molecular Pharmacology, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa 920-1192, Japan. Electronic address: deyama@p.kanazawa-u.ac.jp.
Ronald S DumanDepartment of Psychiatry, Yale University School of Medicine, New Haven, CT 06519, USA.
Kanazawa University · JPYale University · US

Funding

Role of mTOR and Synaptogenesis in the Actions of Rapid-Acting AntidepressantsR01MH093897 · NIMH · YALE UNIVERSITY · PI DILEONE, RALPH J · 2011 to 2021
$5.0M
Antidepressants: Signal Transduction and Gene ExpressionR37MH045481 · NIMH · YALE UNIVERSITY · PI DUMAN, RONALD S. · 2005 to 2014
$3.5M
ANTIDEPRESSANTS AND SIGNAL TRANSDUCTION IN BRAINR01MH045481 · NIMH · YALE UNIVERSITY · PI DUMAN, RONALD S. · 1995 to 2004
$1.3M
NIMH NIH HHS R01 MH045481NIMH NIH HHS R01 MH093897NIMH NIH HHS R37 MH045481
6 · The paper itself

Abstract

Clinical and preclinical studies have demonstrated that depression, one of the most common psychiatric illnesses, is associated with reduced levels of neurotrophic factors, including brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF), contributing to neuronal atrophy in the prefrontal cortex (PFC) and hippocampus, and reduced hippocampal adult neurogenesis. Conventional monoaminergic antidepressants can block/reverse, at least partially, these deficits in part via induction of BDNF and/or VEGF, although these drugs have significant limitations, notably a time lag for therapeutic response and low response rates. Recent studies reveal that ketamine, an N-methyl-d-aspartate receptor antagonist produces rapid (within hours) and sustained (up to a week) antidepressant actions in both patients with treatment-resistant depression and rodent models of depression. Rodent studies also demonstrate that ketamine rapidly increases BDNF and VEGF release and/or expression in the medial PFC (mPFC) and hippocampus, leading to increase in the number and function of spine synapses in the mPFC and enhancement of hippocampal neurogenesis. These neurotrophic effects of ketamine are associated with the antidepressant effects of this drug. Together, these findings provide evidence for a neurotrophic mechanism underlying the rapid and sustained antidepressant actions of ketamine and pave the way for the development of rapid and more effective antidepressants with fewer side effects than ketamine.

Indexed as

AnimalsAntidepressive AgentsBrain-Derived Neurotrophic FactorDepressionHippocampusHumansKetaminePrefrontal CortexTime FactorsVascular Endothelial Growth Factor AAntidepressive AgentsBDNF protein, humanBrain-Derived Neurotrophic FactorKetamineVascular Endothelial Growth Factor AVEGFA protein, humanBDNFDepressionKetamineRapid antidepressantsSynaptogenesisVEGF-A

Identifiers

PMID31830487
PMCPMC6997025
OpenAlexW2996052033

What OpenQuestion holds

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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.