Sustained rescue of prefrontal circuit dysfunction by antidepressant-induced spine formation
Open accessAbstract
Why is ketamine an antidepressant?: A better understanding of the mechanisms underlying the action of antidepressants is urgently needed. Moda-Sava et al. explored a possible mode of action for the drug ketamine, which has recently been shown to help patients recover from depression (see the Perspective by Beyeler). Ketamine rescued behavior in mice that was associated with depression-like phenotypes by selectively reversing stress-induced spine loss and restoring coordinated multicellular ensemble activity in prefrontal microcircuits. The initial induction of ketamine's antidepressant effect on mouse behavior occurred independently of effects on spine formation. Instead, synaptogenesis in the prefrontal region played a critical role in nourishing these effects over time. Interventions aimed at enhancing the survival of restored synapses may thus be useful for sustaining the behavioral effects of fast-acting antidepressants. Science , this issue p. eaat8078 ; see also p. 129
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Activation of AS-PaRac1 three hours post-treatment did not impact tail suspension test behavior 48 hours post-treatment, prior to the onset of spine formation by ketamine at 12 hours post-treatment.
“Activation of AS-PaRac1 three hours post-treatment did not impact tail suspension test behavior 48 hours post-treatment, which is prior to the onset of spine formation by ketamine 12 hours post-treatment.”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Moda-Sava et al., 2019
The Results section on prefrontal spinogenesis reports that activating AS-PaRac1 3 hours after ketamine did not affect immobility behavior when tested 2 days after treatment. It also reports that increased spine formation became detectable at 12–24 hours. The 3-hour activation preceded spine formation, but the sentence incorrectly describes the 48-hour behavioral test as occurring before it. (LLM, conf=0.88)
Experimental — accuracy not yet measuredChronic 21-day corticosterone exposure in mice induces dendritic spine elimination in mPFC, which is rescued 24 hours after a single ketamine treatment at 10 mg/kg i.p.
“Using a chronic (21 day) corticosterone (CORT) exposure model of depression in mice, this study demonstrated that CORT induces dendritic spine elimination in the mPFC which is rescued 24 hours following a single ketamine treatment (10 mg/kg i.p.).”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Moda-Sava et al., 2019
The Results sections report spine loss after chronic CORT exposure, including a 21-day assessment, and imaging 24 hours after a single 10 mg/kg intraperitoneal ketamine dose (page numbers unavailable). Ketamine reversed the effect on spine density, but “rescued” overstates recovery of the eliminated spines: 51.7% of lost spines were not restored, and ketamine did not significantly change spine elimination rates. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe 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 [10]
The Results report that ketamine rescued stress-related spine loss in mice, supporting the neuroplasticity-reversal part of the claim. But the Results section on prefrontal spinogenesis says behavioral effects began at 3 hours, before spine formation increased at 12–24 hours; spine formation was not required for the acute effect. This paper therefore does not support attributing the rapidity of ketamine’s effects to spine restoration, and it does not establish that mechanism as an explanation for their magnitude. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMultiple efficacious therapies often reverse neuroplasticity deficits.
“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 [10]
The Discussion (page not provided) reports that ketamine rescued stress-associated spine loss and prefrontal circuit dysfunction in two mouse models. It does not establish that multiple efficacious therapies reverse neuroplasticity deficits; it discusses other interventions as possibilities rather than demonstrated results. (LLM, conf=0.84)
Experimental — accuracy not yet measuredKetamine and psychedelics modulate cortical neuron function by increasing dendritic spine and synapse density in the PFC.
“Ketamine and psychedelics modulate cortical neuron function by increasing dendritic spine and synapse density in the PFC (129, 146–149)”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [129]
The Results section (‘Antidepressant-dose ketamine selectively restores lost spines’; page not provided) reports that ketamine increased PFC dendritic spine and synapse density. This paper does not establish the claim for psychedelics. Its Results section (‘Prefrontal spinogenesis sustains the remission of depression-related behavior over time’) also reports that ketamine restored circuit activity before spine formation was detectable, so increased spine density was not required to induce the functional change. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Animal studies show that ketamine-induced increases in synaptic proteins and density.
“While animal studies show that ketamine-induced increases in synaptic proteins and density 14 67 40”
From Imaging the effect of ketamine on synaptic density (SV2A) in the living brain (2022) · cites this paper as [40]
In Results, under “Antidepressant-dose ketamine selectively restores lost spines” (page unavailable), ketamine increased dendritic spine density and reversed a reduction in the density of PSD-95 labeling in the mouse prefrontal cortex. PSD-95 is a synaptic protein, but the passage measures the density of its labeling, not an increase in synaptic protein levels generally. (LLM, conf=0.82)
Experimental — accuracy not yet measuredChronic exposure to uncontrollable stress causes loss of spines and dendrites in the prefrontal cortex (PFC).
“Chronic exposure to uncontrollable stress causes loss of spines and dendrites in the prefrontal cortex (PFC), a recently evolved brain region that provides top-down regulation of thought, action, and emotion.”
From Chronic Stress Weakens Connectivity in the Prefrontal Cortex: Architectural and Molecular Changes. (2021) · cites this paper as [77]
The Results (page unavailable) report increased PFC spine elimination after chronic corticosterone exposure and comparable effects after repeated restraint stress. They also note stress-induced dendritic atrophy, but this study does not report measuring loss of dendrites, and it does not characterize the stress as uncontrollable. (LLM, conf=0.85)
Experimental — accuracy not yet measuredKetamine rescued the increase in immobility produced by corticosterone exposure in the tail suspension test from three hours to one week post-treatment.
“ketamine rescued the increase in immobility produced by CORT exposure during the tail suspension test starting at three hours to one-week post-treatment.”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Moda-Sava et al., 2019
Specific deletion of newly formed spines 24 hours post-treatment via AS-PaRac1 reversed ketamine's effects in the tail suspension test 48 hours post-treatment.
“specific deletion of the newly formed spines 24 hours post-treatment via activated synapse-targeting photoactivatable Rac1 (AS-PaRac1), which collapses newly formed spines through light stimulation, reversed the effects of ketamine in the tail suspension test 48 hours post-treatment.”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Moda-Sava et al., 2019
Ketamine restored dendritic spines specifically lost during corticosterone exposure.
“Ketamine restored dendritic spines that were specifically lost during the CORT exposure.”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Moda-Sava et al., 2019
New synapse formation is causally related to the antidepressant actions of ketamine.
“An elegant recent study provided further evidence that new synapse formation is causally related to the antidepressant actions of ketamine 10 .”
From Neuroplasticity in cognitive and psychological mechanisms of depression: an integrative model (2020) · cites this paper as [10]
Ketamine exhibits rapid plasticity-enhancing effects in animal models and rapid clinical effects in human patients.
“As an example, we discuss the potential for ketamine-which exhibits both rapid plasticity-enhancing effects in animal models 4,10 and rapid clinical effects in human patients 11,12 -to provide a test of the predictions of this integrative model, including simultaneous and correlated reversals of multiple plasticity-related deficits across levels of analysis.”
From Neuroplasticity in cognitive and psychological mechanisms of depression: an integrative model (2020) · cites this paper as [10]
Experimental — accuracy not yet measuredThese structural changes are accompanied by depressive phenotypes related to motivation, anxiety, and anhedonia.
“These structural changes are accompanied by depressive phenotypes related to motivation (129), anxiety (122), and anhedonia (122, 129).”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [129]
Ketamine-induced spine growth in the PFC is causally related to long-lasting antidepressant effects of the drug in rodents.
“Liston et al. recently used a photoactivatable Rac1 to demonstrate that ketamine-induced spine growth in the PFC was causally related to long-lasting antidepressant effects of the drug in rodents (129).”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [129]
In both humans and rodents, the antidepressant responses of ketamine appear to last for about 1 week.
“In both humans and rodents, the antidepressant responses of ketamine appear to last for about 1 week.”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [129]
Ketamine regrows the dendritic spines lost to stress in a targeted manner.
“Indeed, recent in vivo work indicates that ketamine regrows the dendritic spines lost to stress in a targeted manner.”
From Imaging the effect of ketamine on synaptic density (SV2A) in the living brain (2022) · cites this paper as [40]
With chronic stress exposure, there is architectural loss of mPFC spines and dendrites that correlates with impaired PFC cognitive functioning.
“With chronic stress exposure, there is architectural loss of mPFC spines and dendrites (Moda-Sava et al., 2019, Radley et al., 2006) that correlates with impaired PFC cognitive functioning (Hains et al., 2009, Hains et al., 2015, Liston et al., 2006).”
From Guanfacine’s mechanism of action in treating prefrontal cortical disorders: Successful translation across species (2020) · cites this paper as Moda-Sava et al., 2019
Computational tools that integrate fMRI and EEG already recover predictive signatures of response and can propose dose and timing schedules aligned to individual network states.
“Computational tools that integrate fMRI and EEG already recover predictive signatures of response and can propose dose and timing schedules aligned to individual network states [14,37,181].”
From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [181]
The Results section describes two-photon calcium imaging and fiber photometry in mice; its prediction concerns a shift from immobility to struggling, not treatment response. Searches for fMRI/EEG integration, predictive response signatures, and individualized dose or timing schedules found no passage addressing the claim. Page numbers were not provided in our copy. (LLM, conf=0.77)
Experimental — accuracy not yet measuredCORT mice showed spine loss in prefrontal microcircuit and altered BDNF signaling and neurogenesis with reduced progenitor cell proliferation in hippocampal and cortical structures.
“Similarly to observation in MDD, CORT mice showed spine loss in prefrontal microcircuit and altered neuronal brain-derived neurotrophic factor (BDNF) signaling and neurogenesis with a reduced progenitor cell proliferation in hippocampal and cortical structures.6,7”
From Synaptic Vesicle 2A (SV2A) Positron Emission Tomography (PET) Imaging as a Marker of Therapeutic Response in a Mouse Model of Depression (2025) · cites this paper as [7]
The induction of antidepressant behavioral effects occurs in vivo independently of (and before) actual spine formation, but glutamate-induced synaptogenesis plays a critical role in sustaining the effects over the subsequent week.
“Second, another study demonstrated that the induction of antidepressant behavioral effects occurs in vivo independently of (and before) actual spine formation. However, glutamate-induced synaptogenesis in their study played a critical role in sustaining the effects over the subsequent week [80].”
From Pharmacotherapies Targeting GABA-Glutamate Neurotransmission for Treatment-Resistant Depression (2023) · cites this paper as [80]
Multiple studies reported ketamine increasing dendritic spine density within 12-24 h.
“Multiple studies have reported similar occurrences with ketamine increasing dendritic spine density within 12–24 h of administration (Li et al., 2010; Liu et al., 2013; Moda-Sava et al., 2019).”
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 Moda-Sava et al., 2019
In a mouse model, chronic corticosterone exposure-induced depression-related behavior correlated with targeted dendritic spine elimination within prefrontal cortex micro-circuits.
“Moda-Sava, et al. [145] used longitudinal imaging to demonstrate that the induction of depression-related behavior by chronic stress in mice, simulated by chronic corticosterone (CORT) exposure, correlated with targeted dendritic spine elimination within prefrontal cortex micro-circuits.”
From Challenges and rewards of in vivo synaptic density imaging, and its application to the study of depression (2025) · cites this paper as [145]
Ketamine treatment selectively restored spines eliminated during CORT exposure.
“while these studies found that ketamine treatment selectively restored spines eliminated during CORT exposure”
From Challenges and rewards of in vivo synaptic density imaging, and its application to the study of depression (2025) · cites this paper as [145]
Spinogenesis may be important for the long-term maintenance of ketamine's behavioral effects.
“suggesting that spinogenesis may be important for the long-term maintenance of these behavioral effects”
From Challenges and rewards of in vivo synaptic density imaging, and its application to the study of depression (2025) · cites this paper as [145]
The degree to which ketamine restored spines eliminated during CORT exposure correlated with the sustained (2 days-1 week) antidepressant response.
“the authors observed a relationship between the degree to which ketamine was able to restore spines eliminated during CORT exposure and the sustained (2 days -1 week) antidepressant response”
From Challenges and rewards of in vivo synaptic density imaging, and its application to the study of depression (2025) · cites this paper as [145]
The effect of ketamine on antidepressant behavior preceded its effects on spine formation.
“the effect of ketamine on antidepressant behavior preceded its effects on spine formation”
From Challenges and rewards of in vivo synaptic density imaging, and its application to the study of depression (2025) · cites this paper as [145]
Spinogenesis is not required for inducing ketamine's effects on behavior.
“suggesting spinogenesis is not required for inducing ketamine's effects on behavior”
From Challenges and rewards of in vivo synaptic density imaging, and its application to the study of depression (2025) · cites this paper as [145]
Ketamine and other fast-acting antidepressants rapidly restore dendritic spine density in the prefrontal cortex of stressed and unstressed animals.
“Ketamine and other fast-acting antidepressant candidates all produce a rapid restoration of dendritic spine density in the PFC in stressed and unstressed animals with the same rapid time course as its behavioral actions [145, 187, 202, 203], implying the restoration of synaptic and circuit function, too.”
From Plasticity of synapses and reward circuit function in the genesis and treatment of depression (2023) · cites this paper as [145]
The time course of ketamine-induced spine restoration matches its behavioral actions.
“Ketamine and other fast-acting antidepressant candidates all produce a rapid restoration of dendritic spine density in the PFC in stressed and unstressed animals with the same rapid time course as its behavioral actions [145, 187, 202, 203], implying the restoration of synaptic and circuit function, too.”
From Plasticity of synapses and reward circuit function in the genesis and treatment of depression (2023) · cites this paper as [145]
Rapid spine restoration implies restoration of synaptic and circuit function.
“Ketamine and other fast-acting antidepressant candidates all produce a rapid restoration of dendritic spine density in the PFC in stressed and unstressed animals with the same rapid time course as its behavioral actions [145, 187, 202, 203], implying the restoration of synaptic and circuit function, too.”
From Plasticity of synapses and reward circuit function in the genesis and treatment of depression (2023) · cites this paper as [145]
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- Authors
- Moda-Sava, R. N., Murdock, M. H., Parekh, P. K., Fetcho, R. N., Huang, B. S., Huynh, T. N., Witztum, J., Shaver, D. C., Rosenthal, D. L., Alway, E. J., Lopez, K., Meng, Y., Nellissen, L., Grosenick, L., Milner, T. A., Deisseroth, K., Bito, H., Kasai, H., & Liston, C.
- Affiliations
- Weill Cornell Medicine (US)
- Stanford University (US)
- The University of Tokyo (JP)
- Center for Disease Biology and Integrative Medicine, The University of Tokyo (JP)
- Corresponding author
- Moda-Sava, R. N.
- Murdock, M. H.
- Parekh, P. K.
- Liston, C.
- ORCID
- Venue
- Science
- Published
- 2019-04-12
- Volume
- 364
- Issue
- 6436
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC6785189
- OpenAlex
- W2935995671
- Cited by
- 643
- References
- 96
- Citations by year
- 2026: 64 · 2025: 92 · 2024: 91 · 2023: 91 · 2022: 91 · 2021: 96 · 2020: 84 · 2019: 34
- FWCI
- 47.26
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Science Foundation
- National Institute of Mental Health (R00 MH097822, R01 MH109685)
- Simons Foundation (429965)
- Whitehall Foundation
- Rita Allen Foundation
- KAKENHI (Grant 17H06312)
- Japan Agency for Medical Research and Development
- Ministry of Education, Culture, Sports, Science, and Technology
- Hartwell Foundation
- One Mind Institute
- Klingenstein-Simons Fellowship in Brain Science
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- depression, antidepressant effects, ketamine, dendritic spine formation, medial prefrontal cortex, postsynaptic neurons
- MeSH terms
- Animals, Antidepressive Agents, Corticosterone, Depressive Disorder, Disease Models, Animal, Escape Reaction, Ketamine, Mice, Inbred C57BL, Mice, Transgenic, Neuronal Plasticity, Stress, Psychological, Synapses, Prefrontal Cortex, Dendritic Spines, Mice
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