Neurotrophic mechanisms underlying the rapid and sustained antidepressant actions of ketamine
Open accessAbstract
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.
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This disinhibition of glutamatergic pyramidal neurons triggers a rapid surge in extracellular glutamate, with notable effects on synaptogenesis.
“This disinhibition of glutamatergic pyramidal neurons triggers a rapid surge in extracellular glutamate, with notable effects on synaptogenesis [44,58].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [44]
The BDNF section reports a rapid increase in extracellular glutamate after low-dose ketamine and links the resulting glutamate burst to pathways involved in synaptogenesis. It describes disinhibition as the proposed mechanism—the burst is “thought to occur” through blockade of NMDARs on inhibitory interneurons—so the claim states that causal step more definitively than the source does. (LLM, conf=0.83)
Experimental — accuracy not yet measuredEvidence on regional variations in BDNF induced by antidepressants is limited, with most findings in hippocampus and PFC.
“there is limited evidence on regional variations in BDNF induced by antidepressants, with most findings highlighting effects in the hippocampus and PFC [44].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [44]
The section on BDNF and VEGF signaling in conventional antidepressant action (page unavailable) reports antidepressant-associated increases in BDNF in the hippocampus and PFC. It does not assess regional variation or state that evidence on such variation is limited, so that part of the claim is unsupported. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe neurotrophic factor theory of depression emerged in part from clinical and preclinical studies showing significant gross structural changes in hippocampus and PFC linked to neuronal atrophy.
“The neurotrophic factor theory of depression, in part, emerged from several clinical and preclinical studies that showed significant gross structural changes in the hippocampus and PFC linked to neuronal atrophy (Deyama & Duman, 2020).”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Deyama & Duman, 2020
At sub-anesthetic doses used for depression, ketamine preferentially blocks NMDA receptors on GABAergic interneurons.
“In contrast, at sub-anesthetic doses used for depression, ketamine preferentially blocks NMDA receptors on GABAergic interneurons [44,58].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [44]
Ketamine has a well-established action on BDNF levels in the prefrontal cortex, which plays a significant role in its antidepressant effects.
“the well-established action of ketamine on BDNF levels in the prefrontal cortex, which plays a significant role in its antidepressant effects [44].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [44]
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Research works printed but not linked: 1
- Navitor, 2019 Navitor’s three phase 1 studies for NV-5138 show antidepressant effects and biomarker impact, supporting further development of direct activator of mTORC1 in depression. http://www.navitorpharma.com/news/press-releases/navitors-three-phase-1-studies-for-nv-5138-show-antidepressant-effects-and-biomarker-impact-supporting-further-development-of-direct-activator-of-mtorc1-in-depression/ (accessed 28 November 2019).
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- Authors
- Deyama, S., & Duman, R. S.
- Affiliations
- Kanazawa University (JP)
- Yale University (US)
- Corresponding author
- Deyama, Satoshi
- Venue
- Pharmacology Biochemistry and Behavior
- Publisher
- Elsevier BV
- Published
- 2020-01
- Volume
- 188
- Pages
- 172837
- ISSN
- 0091-3057 (ISSN-L)
- PMC
- PMC6997025
- OpenAlex
- W2996052033
- Cited by
- 186
- References
- 155
- Citations by year
- 2026: 16 · 2025: 26 · 2024: 28 · 2023: 24 · 2022: 34 · 2021: 38 · 2020: 19 · 2017: 1
- FWCI
- 2.92
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Pharmacology Biochemistry and Behavior (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Shimabara Science Promotion Foundation
- Uehara Memorial Foundation
- Japan Society for the Promotion of Science
- National Institute of Mental Health
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- ketamine, antidepressant mechanism, neurotrophic factors, brain-derived neurotrophic factor, vascular endothelial growth factor, treatment-resistant depression, medial prefrontal cortex, hippocampal neurogenesis, NMDA receptor antagonists, rapid-acting antidepressants, neuronal atrophy
- MeSH terms
- Animals, Antidepressive Agents, Depression, Hippocampus, Humans, Ketamine, Time Factors, Prefrontal Cortex, Brain-Derived Neurotrophic Factor, Vascular Endothelial Growth Factor A
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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