Ketamine and Rapid-Acting Antidepressants: A Window into a New Neurobiology for Mood Disorder Therapeutics
Open accessAbstract
Ketamine is the prototype for a new generation of glutamate-based antidepressants that rapidly alleviate depression within hours of treatment. Over the past decade, there has been replicated evidence demonstrating the rapid and potent antidepressant effects of ketamine in treatment-resistant depression. Moreover, preclinical and biomarker studies have begun to elucidate the mechanism underlying the rapid antidepressant effects of ketamine, offering a new window into the biology of depression and identifying a plethora of potential treatment targets. This article discusses the efficacy, safety, and tolerability of ketamine, summarizes the neurobiology of depression, reviews the mechanisms underlying the rapid antidepressant effects of ketamine, and discusses the prospects for next-generation rapid-acting antidepressants.
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Depression is characterized at the molecular level as a failure of neuroplasticity, including neuronal atrophy and synaptic depression in the medial prefrontal cortex (mPFC) and hippocampus.
“At the molecular level, depression has been characterized as a failure of neuroplasticity, including neuronal atrophy and synaptic depression in the medial prefrontal cortex (mPFC) and hippocampus 3-5 .”
From Neuroplasticity in cognitive and psychological mechanisms of depression: an integrative model (2020) · cites this paper as [3]
The section “Synaptic Homeostasis and the Neurobiology of Depression” links depression to altered synaptic plasticity and reports neuronal atrophy and synaptic depression in the prefrontal cortex and hippocampus. It says prefrontal cortex (PFC), however, without specifying the medial prefrontal cortex (mPFC) as the claim does. Page numbers were not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAttempts to extend molecular findings to humans (e.g., BDNF and synapse levels) have yielded inconsistent results.
“While molecular neuroplasticity effects are well-described in rodent models, attempts to extend molecular findings to humans (e.g., BDNF and synapse levels) have yielded inconsistent results 3 , in no small part because of the difficulty of assessing these endpoints in the living brain, the tissue of interest.”
From Neuroplasticity in cognitive and psychological mechanisms of depression: an integrative model (2020) · cites this paper as [3]
The 'Restoration of Neurotrophic Function' section reports mixed human findings for peripheral BDNF after ketamine: an early study found no relationship with response, while a larger trial found a positive relationship. It discusses an indirect EEG marker of synaptic strength, but does not report similarly inconsistent findings for human synapse levels. (LLM, conf=0.83)
Experimental — accuracy not yet measuredImpairments of neuroplasticity often characterize disorders of negative affect including depression.
“Impairments of neuroplasticity often characterize disorders of negative affect including depression 3,4 and multiple efficacious therapies often reverse such deficits 10,148-151 .”
From Neuroplasticity in cognitive and psychological mechanisms of depression: an integrative model (2020) · cites this paper as [3]
The “Synaptic Homeostasis and the Neurobiology of Depression” section associates depression with neuronal atrophy, reduced synaptic connectivity, and other changes in synaptic plasticity. It supports the claim for depression, but does not establish that these impairments often characterize disorders of negative affect more broadly. Page numbers are not available in the supplied passages. (LLM, conf=0.84)
Experimental — accuracy not yet measuredKetamine administration reverses synaptic loss and depressive-like behavior induced by chronic stress in preclinical models.
“Pioneering preclinical work carried out by Duman et al. indicates that administration of ketamine reverses the synaptic loss and depressive-like behavior induced by chronic stress 15,29,30 .”
From Imaging the effect of ketamine on synaptic density (SV2A) in the living brain (2022) · cites this paper as [30]
The review’s “Synaptogenesis and the Rapid Antidepressant Effects of Ketamine” section (page unavailable) says that ketamine rapidly opposes stress-induced prefrontal neuronal atrophy and synaptic dysconnectivity, and it reports antidepressant effects in rodents. It does not specifically state that ketamine reverses depressive-like behavior induced by chronic stress. (LLM, conf=0.82)
Experimental — accuracy not yet measuredSimilar results in BDNF mRNA and TrkB phosphorylation have been observed after acute treatment with ketamine.
“Similar results in BDNF mRNA and TrkB phosphorylation have been observed after acute treatment with ketamine [216,217,218,219].”
From Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer (2020) · cites this paper as [217]
In “Synaptogenesis and the Rapid Antidepressant Effects of Ketamine” (page unavailable), the review reports increased BDNF translation after acute ketamine treatment. It does not report increased BDNF mRNA or TrkB phosphorylation; the phosphorylation it names is reduced eEF2 phosphorylation. (LLM, conf=0.82)
Experimental — accuracy not yet measured
The rapidity and magnitude of ketamine's antidepressant effects have been attributed to its ability to rapidly reverse neuroplasticity deficits in animal models.
“The rapidity and magnitude of ketamine's effects have been attributed to its ability to rapidly reverse neuroplasticity deficits in animal models 3,4,10,34 .”
From Neuroplasticity in cognitive and psychological mechanisms of depression: an integrative model (2020) · cites this paper as [3]
Molecular neuroplasticity effects are well-described in rodent models.
“While molecular neuroplasticity effects are well-described in rodent models, attempts to extend molecular findings to humans (e.g., BDNF and synapse levels) have yielded inconsistent results 3 , in no small part because of the difficulty of assessing these endpoints in the living brain, the tissue of interest.”
From Neuroplasticity in cognitive and psychological mechanisms of depression: an integrative model (2020) · cites this paper as [3]
NMDAR antagonist ketamine produces rapid antidepressant effects in treatment-resistant depression.
“The NMDAR antagonist ketamine produces rapid antidepressant effects in those with treatment-resistant depression 221”
From Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications (2022) · cites this paper as [221]
Ketamine's therapeutic efficacy appears dependent upon its effects on PFC, along with connecting regions.
“and its therapeutic efficacy appears to be dependent upon its effects on PFC, along with its connecting regions.”
From Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications (2022) · cites this paper as [221]
A single subanesthetic dose of ketamine produces rapid and long-lasting antidepressant effects even in treatment-resistant patients.
“recent studies demonstrate that a single, subanesthetic dose of ketamine produces rapid (within hours) and long-lasting (7 to 10 days) antidepressant effects even in patients who have failed to respond to traditional antidepressants and are considered treatment resistant (5, 6).”
From Sestrin modulator NV-5138 produces rapid antidepressant effects via direct mTORC1 activation (2019) · cites this paper as [5]
Fast-acting antidepressants such as ketamine produce rapid synaptic changes in the mPFC that are associated with their antidepressant behavioral actions.
“Fast-acting antidepressants such as ketamine also produce rapid synaptic changes in the mPFC that are associated with the antidepressant behavioral actions of these agents (45).”
From Sestrin modulator NV-5138 produces rapid antidepressant effects via direct mTORC1 activation (2019) · cites this paper as [45]
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Serial infusions of low-dose ketamine for major depression
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Potential Psychiatric Applications of Metabotropic Glutamate Receptor Agonists and Antagonists
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mTOR activation is required for the antidepressant effects of mGluR2/3 blockade
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Self-citationEffects of Ketamine in Treatment-Refractory Obsessive-Compulsive Disorder
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On the safety and benefits of repeated intravenous injections of ketamine for depression.
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Vitamin B12 Level may be Related to the Efficacy of Single Ketamine Infusion in Bipolar Depression
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Self-citationAntidepressant drugs act by directly binding to TRKB neurotrophin receptors
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“depressant effects in those with treatment-resistant depression [221], and its therapeutic efficacy appears to be”
BackgroundKetamine Treatment and Global Brain Connectivity in Major Depression
Abdallah, C. G., Averill, L. A., Collins, K. A., Geha, P., Schwartz, J., Averill, C., DeWilde, K. E., Wong, E., Anticevic, A., Tang, C. Y., et al. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2016.186 · Cited by 300 · see citing works
Self-citationNeuronal plasticity and neurotrophic factors in drug responses
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Neuroplasticity as a convergent mechanism of ketamine and classical psychedelics
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Ketamine: NMDA Receptors and Beyond
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Psychedelics in Psychiatry: Neuroplastic, Immunomodulatory, and Neurotransmitter Mechanisms
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Clinical applications of hallucinogens: a review
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The stressed synapse 2.0: pathophysiological mechanisms in stress-related neuropsychiatric disorders
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Neurotrophic mechanisms underlying the rapid and sustained antidepressant actions of ketamine
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Self-citationKynurenine pathway metabolites and suicidality
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Reduced global functional connectivity of the medial prefrontal cortex in major depressive disorder
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Self-citationNeuropeptide and small transmitter coexistence: Fundamental studies and relevance to mental illness
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A phase 2 trial of inhaled nitrous oxide for treatment-resistant major depression
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The Nucleus Accumbens and Ketamine Treatment in Major Depressive Disorder
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Self-citationThe molecular pathophysiology of depression and the new therapeutics
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BDNF Release and Signaling Are Required for the Antidepressant Actions of GLYX-13
Kato, T., Fogaça, M. V., Deyama, S., Li, X.-Y., Fukumoto, K., & Duman, R. S. (2018) · Molecular Psychiatry · doi:10.1038/mp.2017.220 · Cited by 88 · see citing works
Self-citationSestrin modulator NV-5138 produces rapid antidepressant effects via direct mTORC1 activation
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iPlasticity: Induced juvenile‐like plasticity in the adult brain as a mechanism of antidepressants
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Imaging the effect of ketamine on synaptic density (SV2A) in the living brain
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“Given the doseresponse relationship between the glutamate surge, synaptogenesis, and antidepressant response following ketamine administration [28, 30, 54], it is possible that the relationship between derealization and increased SV2A density observed here is mediated by glutamate release.”
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Cyclooxygenase-2 inhibition reduces stress-induced affective pathology
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A preliminary study of adjunctive ketamine for treatment-resistant bipolar depression
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Self-citationKetamine vs midazolam: Mood improvement reduces suicidal ideation in depression
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Astroglial Serotonin Receptors as the Central Target of Classic Antidepressants
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The role of reelin in the pathological mechanism of depression from clinical to rodents
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Serotonergic psychedelics for depression: A comprehensive overview
Wingert, A. M., Agnorelli, C., Peill, J., Reed, S., Nutt, D. J., & Erritzoe, D. (2025) · International Review of Neurobiology · doi:10.1016/bs.irn.2025.04.009 · Cited by 2 · see citing works
- Authors
- Abdallah, C. G., Sanacora, G., Duman, R. S., & Krystal, J. H.
- Affiliations
- Yale University (US)
- Venue
- Annual Review of Medicine
- Publisher
- Annual Reviews
- Published
- 2015-01-14
- Volume
- 66
- Issue
- 1
- Pages
- 509-523
- ISSN
- 0066-4219 (ISSN-L)
- 1545-326X
- PMC
- PMC4428310
- OpenAlex
- W2108057532
- Cited by
- 422
- References
- 110
- Citations by year
- 2026: 30 · 2025: 31 · 2024: 31 · 2023: 25 · 2022: 51 · 2021: 43 · 2020: 36 · 2019: 32 · 2018: 37 · 2017: 44 · 2016: 38 · 2015: 24
- FWCI
- 4.53
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs
- State of Connecticut Department of Mental Health and Addiction Services
- National Institutes of Health (5k23mh101498-05)
- National Center for PTSD, U.S. Department of Veterans Affairs
- National Institute of Mental Health (K23MH-101498(, R01MH081211, MH 17871, MH081211, MH093897, R01MH093897, R37MH017871, MH101498, R01MH017871, R01MH105910)
- National Center for Research Resources (UL1RR024139)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Health Sciences › Medicine › Psychiatry and Mental health › Electroconvulsive Therapy Studies
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- ketamine, rapid-acting antidepressants, treatment-resistant depression, antidepressant mechanism, biomarkers, drug safety and tolerability
- MeSH terms
- Antidepressive Agents, Brain, Major Depressive Disorder, Humans, Ketamine, Neuronal Plasticity, Prefrontal Cortex, Excitatory Amino Acid Antagonists, Glutamic Acid, Mood Disorders, Depressive Disorder, Treatment-Resistant
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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