Evidence map›Paper›PMID 32017978›Full record

ReviewBehavioural brain research2020

Ketamine: The final frontier or another depressing end?

Omar K Sial, Eric M Parise, Lyonna F Parise, Tamara Gnecco, Carlos A Bolaños-Guzmán

Open access · greenAbstract readReview
In one paragraph

Review in Behavioural brain research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Ketamine and Evolving Neuroplasticity.Clinical drug investigation · 2026
    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

5 authors at 2 institutions in 1 country.

Omar K SialTexas A&M University: Department of Psychological and Brain Sciences, 4325 TAMU, College Station, TX, 77843, USA.
Eric M PariseFishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Place, New York, NY, 10029, USA.
Lyonna F PariseFishberg Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Place, New York, NY, 10029, USA.
Tamara GneccoTexas A&M University: Department of Psychological and Brain Sciences, 4325 TAMU, College Station, TX, 77843, USA.
Carlos A Bolaños-GuzmánTexas A&M University: Department of Psychological and Brain Sciences, 4325 TAMU, College Station, TX, 77843, USA. Electronic address: bolanos@tamu.edu.
Texas A&M University · USAllen Institute for Brain Science · US

Funding

Serotonin receptors that potentiate addiction-related behavioral and molecular effects induced by methylphenidate plus SSRI exposureR01DA046794 · NIDA · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI BOLANOS, CARLOS A., STEINER, HEINZ · 2019 to 2023
$1.7M
NIDA NIH HHS R01 DA046794
6 · The paper itself

Abstract

Two decades ago, the observation of a rapid and sustained antidepressant response after ketamine administration provided an exciting new avenue in the search for more effective therapeutics for the treatment of clinical depression. Research elucidating the mechanism(s) underlying ketamine's antidepressant properties has led to the development of several hypotheses, including that of disinhibition of excitatory glutamate neurons via blockade of N-methyl-d-aspartate (NMDA) receptors. Although the prominent understanding has been that ketamine's mode of action is mediated solely via the NMDA receptor, this view has been challenged by reports implicating other glutamate receptors such as AMPA, and other neurotransmitter systems such as serotonin and opioids in the antidepressant response. The recent approval of esketamine (Spravato™) for the treatment of depression has sparked a resurgence of interest for a deeper understanding of the mechanism(s) underlying ketamine's actions and safe therapeutic use. This review aims to present our current knowledge on both NMDA and non-NMDA mechanisms implicated in ketamine's response, and addresses the controversy surrounding the antidepressant role and potency of its stereoisomers and metabolites. There is much that remains to be known about our understanding of ketamine's antidepressant properties; and although the arrival of esketamine has been received with great enthusiasm, it is now more important than ever that its mechanisms of action be fully delineated, and both the short- and long-term neurobiological/functional consequences of its treatment be thoroughly characterized.

Indexed as

Antidepressive AgentsDepressive Disorder, Treatment-ResistantDopamine Plasma Membrane Transport ProteinsExcitatory Amino Acid AntagonistsHumansKetamineMajor Depressive DisorderNorepinephrine Plasma Membrane Transport ProteinsReceptor, Muscarinic M1Receptors, AMPAReceptors, Dopamine D2Receptors, N-Methyl-D-AspartateReceptors, Opioid, deltaReceptors, Opioid, kappaReceptors, Opioid, muReceptors, Serotonin, 5-HT3Antidepressive AgentsDopamine Plasma Membrane Transport ProteinsEsketamineExcitatory Amino Acid AntagonistsKetamineNorepinephrine Plasma Membrane Transport ProteinsReceptor, Muscarinic M1Receptors, AMPAReceptors, Dopamine D2Receptors, N-Methyl-D-AspartateReceptors, Opioid, deltaReceptors, Opioid, kappaReceptors, Opioid, muReceptors, Serotonin, 5-HT3Receptors, sigmaSerotonin Plasma Membrane Transport ProteinsAntidepressant mechanismDepressionKetamineMajor Depressive DisorderNMDANon-NMDA mechanismRapid antidepressantSpravato

Identifiers

PMID32017978
PMCPMC7127859
OpenAlexW3004131643

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.