Role of BDNF in the Pathophysiology and Treatment of Depression: Activity-Dependent Effects Distinguish Rapid-Acting Antidepressants
Open accessAbstract
The pathophysiology and treatment of depression have been the focus of intense research and while there is much that remains unknown, modern neurobiological approaches are making progress. This work demonstrates that stress and depression are associated with atrophy of neurons and reduced synaptic connectivity in brain regions such as the hippocampus and prefrontal cortex that contribute to depressive behaviors, and conversely that antidepressant treatment can reverse these deficits. The role of neurotrophic factors, particularly brain‐derived neurotrophic factor (BDNF), has been of particular interest as these factors play a key role in activity‐dependent regulation of synaptic plasticity. Here, we review the literature demonstrating that exposure to stress and depression decreases BDNF expression in the hippocampus and PFC and conversely that antidepressant treatment can up‐regulate BDNF in the adult brain and reverse the effects of stress. We then focus on rapid‐acting antidepressants, particularly the NMDA receptor antagonist ketamine, which produces rapid synaptic and antidepressant behavioral actions that are dependent on activity‐dependent release of BDNF. This rapid release of BDNF differs from typical monoaminergic agents that require chronic administration to produce a slow induction of BDNF expression, consistent with the time lag for the therapeutic action of these agents. We review evidence that other classes of rapid‐acting agents also require BDNF release, demonstrating that this is a common, convergent downstream mechanism. Finally, we discuss evidence that the actions of ketamine are also dependent on another growth factor, vascular endothelial growth factor (VEGF) and its complex interplay with BDNF.
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Stress skews synaptic plasticity and intrinsic excitability, degrading cortical and reward circuit function, while rapid-acting and conventional antidepressants restore synaptic strength, spine architecture, and network communication through metaplastic and homeostatic programs that prime future adaptation rather than a single static endpoint.
“Stress skews both, degrading cortical and reward circuit function, while rapid-acting and conventional antidepressants restore synaptic strength, spine architecture, and network communication through metaplastic and homeostatic programs that prime future adaptation rather than a single static endpoint [33,390].”
From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [390]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredTraditional antidepressants increase BDNF levels both peripherally and in targeted brain regions.
“traditional antidepressants, which have been shown to increase BDNF levels both peripherally and in targeted brain regions.”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [2]
The Introduction section on typical antidepressants reports increased BDNF expression in the hippocampus and prefrontal cortex after chronic antidepressant administration. The passages do not report an increase in peripheral BDNF levels, so that part of the claim is unsupported by our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredChronic stress decreases BDNF expression in the hippocampus and prefrontal cortex, contributing to neuronal atrophy observed in depression.
“Chronic stress, a well-established risk factor for MDD, has been shown to decrease BDNF expression in critical brain regions such as the hippocampus and prefrontal cortex (PFC), contributing to the neuronal atrophy observed in depression [2,22,33].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [2]
The Introduction’s “Role of BDNF in stress and depression” section reports that chronic stress decreases BDNF expression in the hippocampus and PFC and causes neuronal atrophy there. It describes reduced BDNF signaling as a possible contributor to the reduced brain volume seen in depressed patients, rather than establishing that causal link as fact. The supplied passages do not specify page numbers. (LLM, conf=0.86)
Experimental — accuracy not yet measuredBDNF is critical for synaptic plasticity, neurogenesis, and neuronal survival, and its altered expression is implicated in the development of depressive symptoms.
“BDNF is critical for synaptic plasticity, neurogenesis, and neuronal survival, and its altered expression has been implicated in the development of depressive symptom [2,22].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [2]
The Introduction sections “Neurobiology of BDNF” and “Role of BDNF in stress and depression” describe BDNF’s roles in synaptic plasticity and neuronal survival, and link altered BDNF expression or signaling to depression. They do not directly establish that BDNF is critical for neurogenesis; that part appears only indirectly in a cited study’s title in the References. No page numbers are available in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredIn the mPFC, BDNF strengthens synaptic connectivity, supporting rapid and long-term synaptic adaptations.
“In the mPFC, BDNF strengthens synaptic connectivity, supporting both rapid and long-term synaptic adaptations [2].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [2]
The section on rapid-acting antidepressants reports that BDNF-dependent signaling is required for ketamine-induced increases in the number and function of mPFC synapses, supporting the rapid-adaptation part of the claim. The copy does not establish that these BDNF-dependent mPFC synaptic changes are long-term; its discussion of long-lasting effects concerns ketamine’s effects rather than the duration of those synaptic changes. Page numbers were not available in the indexed passages. (LLM, conf=0.84)
Experimental — accuracy not yet measured
In the hippocampus, particularly dentate gyrus and CA3, increased BDNF promotes neurogenesis and synaptic plasticity, leading to enhanced mood regulation.
“in the hippocampus, particularly in the dentate gyrus and CA3 regions, increased BDNF promotes neurogenesis and synaptic plasticity, leading to enhanced mood regulation [2].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [2]
The Introduction’s “Role of BDNF in stress and depression” section (page unavailable) links BDNF to synaptic plasticity and reports that hippocampal BDNF knockdown can cause depressive behaviors. It mentions CA3 atrophy under stress, but does not establish that increased BDNF promotes neurogenesis in the dentate gyrus and CA3 or that this chain enhances mood regulation. The dentate-gyrus passage concerns VEGF, not BDNF. (LLM, conf=0.85)
Experimental — accuracy not yet measuredPostmortem PFC of human subjects with Major Depressive Disorder has reduced levels of BDNF, elevated levels of REDD1, and decreased levels of mTOR.
“postmortem PFC of human subjects with Major Depressive Disorder (MDD), similar to stressed rodents, have reduced levels of BDNF,168–173 elevated levels of REDD1,92 and decreased levels of mTOR.92,169”
From Chronic Stress Weakens Connectivity in the Prefrontal Cortex: Architectural and Molecular Changes. (2021) · cites this paper as [168]
The Introduction’s “Role of BDNF in stress and depression” section reports reduced BDNF in postmortem cerebral cortex of depressed subjects, supporting the BDNF portion, though it does not specify PFC for that finding. The passages do not report elevated REDD1 or decreased mTOR in postmortem PFC; the citing sentence attaches a separate citation to REDD1. (LLM, conf=0.86)
Experimental — accuracy not yet measuredConventional antidepressants, including SSRIs, gradually increase BDNF levels with chronic treatment, which correlates with their delayed therapeutic onset.
“Conventional antidepressants, including selective serotonin reuptake inhibitors (SSRIs), have been shown to gradually increase BDNF levels with chronic treatment, which correlates with their delayed therapeutic onset [2,7].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [2]
There are regional variations in BDNF expression.
“there are regional variations in BDNF expression [2].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [2]
BDNF is critical for neuroplasticity, synaptic transmission, and neuronal survival.
“Brain-derived neurotrophic factor (BDNF) is critical for neuroplasticity, synaptic transmission, and neuronal survival.”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [2]
While chronic stress generally suppresses BDNF expression in the hippocampus and PFC, it can increase BDNF levels in the nucleus accumbens and amygdala.
“Interestingly, while chronic stress generally suppresses BDNF expression in the hippocampus and PFC, it can increase BDNF levels in other brain regions, such as the nucleus accumbens and amygdala, where this increased activity may influence the synaptic plasticity associated with depressive symptoms [2].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [2]
The neurotrophic hypothesis of depression suggests that reduced BDNF levels in key brain regions such as hippocampus and prefrontal cortex contribute to neuronal atrophy and synaptic dysfunction in MDD, leading to depressive symptoms.
“The neurotrophic hypothesis of depression suggests that reduced BDNF levels in key brain regions, such as the hippocampus and prefrontal cortex, contribute to the neuronal atrophy and synaptic dysfunction observed in MDD, which in turn leads to the manifestation of depressive symptoms [2,3].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [2]
The rate of activity-dependent BDNF release appears to distinguish rapid-acting agents from their monoaminergic counterparts, whose delayed treatment response coincides with an indirect increase in BDNF secretion weeks after initiation.
“Importantly, the rate of activity-dependent BDNF release appears to distinguish rapid-acting agents discussed in this review from their monoaminergic counterparts, whose delayed treatment response coincides with an indirect increase in BDNF secretion weeks after initiation [53].”
From Pharmacotherapies Targeting GABA-Glutamate Neurotransmission for Treatment-Resistant Depression (2023) · cites this paper as [53]
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BDNF Release and Signaling Are Required for the Antidepressant Actions of GLYX-13
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Self-citationThe Genetics of Major Depression
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Research works printed but not linked: 1
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Brain-Derived Neurotrophic Factor Signaling in Depression and Antidepressant Action
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Psychedelics and Other Psychoplastogens for Treating Mental Illness.
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Chronic Stress Weakens Connectivity in the Prefrontal Cortex: Architectural and Molecular Changes.
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Self-citationKetamine and the Future of Rapid-Acting Antidepressants
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Pharmacotherapies Targeting GABA-Glutamate Neurotransmission for Treatment-Resistant Depression
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“Further caveats to this hypothesis exist as well, and it is important to place any BDNF-related findings within the context of population heterogeneity and neuro-regional specificity [50,53].”
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The role of the brain renin-angiotensin system (RAS) in mild traumatic brain injury (TBI)
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Role of Glial Cells in Neuronal Function, Mood Disorders, and Drug Addiction
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Inozemtseva, L. S., Yatsenko, K. A., Glazova, N. Y., Kamensky, A. A., Myasoedov, N. F., Levitskaya, N. G., Grivennikov, I. A., & Dolotov, O. V. (2024) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2024.177068 · Cited by 4 · see citing works
Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery
Tanaka, M. (2026) · Biomedicines · doi:10.3390/biomedicines14061265
- Authors
- Duman, R. S., Deyama, S., & Fogaça, M. V.
- Affiliations
- Yale University (US)
- Kanazawa University (JP)
- Corresponding author
- Duman, Ronald S.
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 2019-12-20
- Volume
- 53
- Issue
- 1
- Pages
- 126-139
- ISSN
- 0953-816X (ISSN-L)
- 1460-9568
- PMC
- PMC7274898
- OpenAlex
- W2992679405
- Cited by
- 321
- References
- 121
- Citations by year
- 2026: 35 · 2025: 44 · 2024: 68 · 2023: 55 · 2022: 52 · 2021: 44 · 2020: 22 · 2017: 1
- FWCI
- 3.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- European Journal of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (MH045481, MH093897)
- State of Connecticut Department of Mental Health and Addiction Services
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- brain-derived neurotrophic factor, depression, rapid-acting antidepressants, ketamine, NMDA receptor antagonists, stress, hippocampus, prefrontal cortex, synaptic plasticity, neurotrophic factors, vascular endothelial growth factor, antidepressant mechanism
- MeSH terms
- Antidepressive Agents, Depression, Ketamine, Brain-Derived Neurotrophic Factor, Vascular Endothelial Growth Factor A
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