KETAMINE'S MECHANISM OF ACTION: A PATH TO RAPID‐ACTING ANTIDEPRESSANTS
Open accessAbstract
Major depressive disorder (MDD) is a common and debilitating psychiatric disorder. Traditional antidepressants are of limited efficacy and take weeks to months to yield full therapeutic effects. Thus, there is a clear need for effective rapid-acting antidepressant medications. The N-methyl-d-aspartate receptor (NMDA-R) antagonist, ketamine, has received a great deal of attention over the last 20 years due to the discovery that a single subanesthetic dose leads to a rapid antidepressant effect in individuals with treatment-resistant depression. Animal and human research suggest that ketamine's antidepressant effects are mediated by a glutamate surge that leads to a cascade of events that result in synaptogenesis and reversal of the negative effects of chronic stress and depression, particularly within the prefrontal cortex (PFC). Preclinical and clinical data have provided compelling insights into the mechanisms underlying the rapid-acting antidepressant effects of ketamine. This review discusses stress-related neurobiology of depression and the safety, tolerability, and efficacy of ketamine for MDD, along with a review of ketamine's mechanism of action and prospective predictors of treatment response. Research limitations and future clinical prospects are also discussed.
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Early work suggests ketamine may normalize low-baseline SV2A signal, linking circuit plasticity to presynaptic stabilization.
“Proof-of-concept data demonstrate partial recovery after fluoxetine in a depression model, and early work suggests ketamine may normalize low-baseline SV2A signal, linking circuit plasticity to presynaptic stabilization [167,217,218].”
From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [167]
The Antidepressant Mechanism of Action section describes ketamine-related synaptogenesis and increased synaptic strength, supporting the general plasticity component. It does not report SV2A measurements, normalization of a low-baseline SV2A signal, or presynaptic stabilization; searches for those terms returned no such passage. Page numbers were not available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAt subanesthetic doses, ketamine induces a paradoxical increase in glutamate neurotransmission.
“At subanesthetic doses, ketamine induces a paradoxical increase in glutamate neurotransmission [14,49].”
From The effects of ketamine on prefrontal glutamate neurotransmission in healthy and depressed subjects (2018) · cites this paper as [49]
Proof-of-concept data demonstrate partial recovery after fluoxetine in a depression model.
“Proof-of-concept data demonstrate partial recovery after fluoxetine in a depression model, and early work suggests ketamine may normalize low-baseline SV2A signal, linking circuit plasticity to presynaptic stabilization [167,217,218].”
From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [167]
The Synaptic Plasticity and the Neurobiology of Depression section discusses effects of monoaminergic antidepressants generally, but does not report partial recovery after fluoxetine in a depression model. Searches for fluoxetine and partial recovery found no passage addressing that result; a search for SV2A likewise found no passage supporting the other clause of the citing sentence. Page numbers were unavailable in our copy. (LLM, conf=0.74)
Experimental — accuracy not yet measuredThe antidepressant action of S-ketamine is chiefly thought to be mediated through NMDA-R antagonism, causing a glutamate burst that stimulates various actors promoting synaptogenesis.
“The antidepressant action is chiefly thought to be mediated through N-methyl-D-aspartate receptor (NMDA-R) antagonism, as S-ketamine is an NMDA-R antagonist, causing a glutamate burst stimulating various actors that promote synaptogenesis (Abdallah et al., 2016; Shinohara et al., 2021).”
From A single subanaesthetic dose of the rapid-acting antidepressant S-ketamine raises presynaptic SV2A density in limbic regions of the Wistar Kyoto rat model of depression (2024) · cites this paper as Abdallah et al., 2016
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Self-citationHippocampal volume and the rapid antidepressant effect of ketamine
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Self-citationOn the safety and benefits of repeated intravenous injections of ketamine for depression.
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Applications of Deuterium in Medicinal Chemistry
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Self-citationKetamine’s rapid antidepressant effects are mediated by Ca2+-permeable AMPA receptors
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A Decade of Deuteration in Medicinal Chemistry
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Self-citationRapid acting antidepressants in the mTOR pathway: Current evidence
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- Authors
- Abdallah, C. G., Adams, T. G., Kelmendi, B., Esterlis, I., Sanacora, G., & Krystal, J. H.
- Affiliations
- Yale University (US)
- Corresponding author
- Abdallah, Chadi G.
- ORCID
- Venue
- Depression and Anxiety
- Publisher
- Wiley
- Published
- 2016-04-06
- Volume
- 33
- Issue
- 8
- Pages
- 689-697
- ISSN
- 1091-4269 (ISSN-L)
- 1520-6394
- PMC
- PMC4961540
- OpenAlex
- W2337615202
- Cited by
- 206
- References
- 95
- Citations by year
- 2026: 15 · 2025: 14 · 2024: 22 · 2023: 15 · 2022: 25 · 2021: 19 · 2020: 21 · 2019: 18 · 2018: 28 · 2017: 21 · 2016: 7
- FWCI
- 2.83
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Depression and Anxiety (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- U.S. Department of Defense
- American Psychiatric Foundation
- Robert E. Leet and Clara Guthrie Patterson Trust
- 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, major depressive disorder, treatment-resistant depression, NMDA receptor antagonism, synaptogenesis, chronic stress, prefrontal cortex, predictors of treatment response
- MeSH terms
- Animals, Antidepressive Agents, Depressive Disorder, Major, Major Depressive Disorder, Humans, Ketamine, Receptors, N-Methyl-D-Aspartate, Excitatory Amino Acid Antagonists
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