ArticleThe American journal of psychiatry2019
Role of Neuronal VEGF Signaling in the Prefrontal Cortex in the Rapid Antidepressant Effects of Ketamine.
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Article in The American journal of psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.
- The Mechanisms Behind Rapid Antidepressant Effects of Ketamine: A Systematic Review With a Focus on Molecular Neuroplasticity.Frontiers in psychiatry · 2022Pooled it
- Changes in RNA expression levels during antidepressant treatment: a systematic review.Journal of neural transmission (Vienna, Austria : 1996) · 2021Pooled it
- RTMS Mitigates Simulated Spaceflight-Induced Emotional Dysfunction Through VEGFR-2-Mediated Neuroprotection.Brain and behavior · 2026Article
- Ginsenoside Rh2 Protects Against Glutamate-Induced Neurotoxicity in PC12 Cells via Activation of the VEGF-mediated PI3K/Akt/mTOR Signaling Pathway.Neurochemical research · 2026Article
- Methylone promotes neurite outgrowth and has long-lasting effects on fear extinction learning.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
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- Genome-wide methylome-based molecular pathologies associated with depression and suicide.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Review
- Ketamine and its two enantiomers in anesthesiology and psychiatry: A historical review and future directions.Journal of anesthesia and translational medicine · 2024Review
- The role of mGluR5 on the therapeutic effects of ketamine in Wistar rats.Psychopharmacology · 2024Article
- Neuron-specific deletion of VEGF or its receptor Flk-1 occludes the antidepressant-like effects of desipramine and fluoxetine in mice.Neuropsychopharmacology reports · 2024Article
- Ketamine ameliorates activity-based anorexia of adolescent female mice through changes in GluN2B-containing NMDA receptors at postsynaptic cytoplasmic locations of pyramidal neurons and interneurons of medial prefrontal cortex.Brain structure & function · 2024Article
- The endogenous opioid system in the medial prefrontal cortex mediates ketamine's antidepressant-like actions.Translational psychiatry · 2024Article
- The role of neurotrophic factors in novel, rapid psychiatric treatments.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Review
- The endogenous opioid system in the medial prefrontal cortex mediates ketamine's antidepressant-like actions.Research square · 2023Article
- Ketamine and the Disinhibition Hypothesis: Neurotrophic Factor-Mediated Treatment of Depression.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Intranasal Administration of Resolvin E1 Produces Antidepressant-Like Effects via BDNF/VEGF-mTORC1 Signaling in the Medial Prefrontal Cortex.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Article
- From microRNA to protein, linking the neurotrophic hypothesis of depression to the Wistar Kyoto rat.Neuroscience applied · 2023Article
- Review
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Authors and funding
11 authors at 1 institution in 1 country.
Satoshi DeyamaDepartment of Psychiatry, Yale University School of Medicine, New Haven, Conn. (Deyama, Bang, Wohleb, Li, Kato, Gerhard, Dutheil, Dwyer, Taylor, Picciotto, Duman); Laboratory of Molecular Pharmacology, Institute of Medical, Pharmaceutical, and Health Sciences, Kanazawa University, Kanazawa, Japan (Deyama); Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati (Wohleb); Drug Development Research Laboratories, Sumitomo Dainippon Pharma, Suita, Japan (Kato).
Eunyoung BangDepartment of Psychiatry, Yale University School of Medicine, New Haven, Conn. (Deyama, Bang, Wohleb, Li, Kato, Gerhard, Dutheil, Dwyer, Taylor, Picciotto, Duman); Laboratory of Molecular Pharmacology, Institute of Medical, Pharmaceutical, and Health Sciences, Kanazawa University, Kanazawa, Japan (Deyama); Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati (Wohleb); Drug Development Research Laboratories, Sumitomo Dainippon Pharma, Suita, Japan (Kato).
Eric S WohlebDepartment of Psychiatry, Yale University School of Medicine, New Haven, Conn. (Deyama, Bang, Wohleb, Li, Kato, Gerhard, Dutheil, Dwyer, Taylor, Picciotto, Duman); Laboratory of Molecular Pharmacology, Institute of Medical, Pharmaceutical, and Health Sciences, Kanazawa University, Kanazawa, Japan (Deyama); Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati (Wohleb); Drug Development Research Laboratories, Sumitomo Dainippon Pharma, Suita, Japan (Kato).
Xiao-Yuan LiDepartment of Psychiatry, Yale University School of Medicine, New Haven, Conn. (Deyama, Bang, Wohleb, Li, Kato, Gerhard, Dutheil, Dwyer, Taylor, Picciotto, Duman); Laboratory of Molecular Pharmacology, Institute of Medical, Pharmaceutical, and Health Sciences, Kanazawa University, Kanazawa, Japan (Deyama); Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati (Wohleb); Drug Development Research Laboratories, Sumitomo Dainippon Pharma, Suita, Japan (Kato).
Taro KatoDepartment of Psychiatry, Yale University School of Medicine, New Haven, Conn. (Deyama, Bang, Wohleb, Li, Kato, Gerhard, Dutheil, Dwyer, Taylor, Picciotto, Duman); Laboratory of Molecular Pharmacology, Institute of Medical, Pharmaceutical, and Health Sciences, Kanazawa University, Kanazawa, Japan (Deyama); Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati (Wohleb); Drug Development Research Laboratories, Sumitomo Dainippon Pharma, Suita, Japan (Kato).
Danielle M GerhardDepartment of Psychiatry, Yale University School of Medicine, New Haven, Conn. (Deyama, Bang, Wohleb, Li, Kato, Gerhard, Dutheil, Dwyer, Taylor, Picciotto, Duman); Laboratory of Molecular Pharmacology, Institute of Medical, Pharmaceutical, and Health Sciences, Kanazawa University, Kanazawa, Japan (Deyama); Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati (Wohleb); Drug Development Research Laboratories, Sumitomo Dainippon Pharma, Suita, Japan (Kato).
Sophie DutheilDepartment of Psychiatry, Yale University School of Medicine, New Haven, Conn. (Deyama, Bang, Wohleb, Li, Kato, Gerhard, Dutheil, Dwyer, Taylor, Picciotto, Duman); Laboratory of Molecular Pharmacology, Institute of Medical, Pharmaceutical, and Health Sciences, Kanazawa University, Kanazawa, Japan (Deyama); Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati (Wohleb); Drug Development Research Laboratories, Sumitomo Dainippon Pharma, Suita, Japan (Kato).
Jason M DwyerDepartment of Psychiatry, Yale University School of Medicine, New Haven, Conn. (Deyama, Bang, Wohleb, Li, Kato, Gerhard, Dutheil, Dwyer, Taylor, Picciotto, Duman); Laboratory of Molecular Pharmacology, Institute of Medical, Pharmaceutical, and Health Sciences, Kanazawa University, Kanazawa, Japan (Deyama); Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati (Wohleb); Drug Development Research Laboratories, Sumitomo Dainippon Pharma, Suita, Japan (Kato).
Seth R TaylorDepartment of Psychiatry, Yale University School of Medicine, New Haven, Conn. (Deyama, Bang, Wohleb, Li, Kato, Gerhard, Dutheil, Dwyer, Taylor, Picciotto, Duman); Laboratory of Molecular Pharmacology, Institute of Medical, Pharmaceutical, and Health Sciences, Kanazawa University, Kanazawa, Japan (Deyama); Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati (Wohleb); Drug Development Research Laboratories, Sumitomo Dainippon Pharma, Suita, Japan (Kato).
Marina R PicciottoDepartment of Psychiatry, Yale University School of Medicine, New Haven, Conn. (Deyama, Bang, Wohleb, Li, Kato, Gerhard, Dutheil, Dwyer, Taylor, Picciotto, Duman); Laboratory of Molecular Pharmacology, Institute of Medical, Pharmaceutical, and Health Sciences, Kanazawa University, Kanazawa, Japan (Deyama); Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati (Wohleb); Drug Development Research Laboratories, Sumitomo Dainippon Pharma, Suita, Japan (Kato).
Ronald S DumanDepartment of Psychiatry, Yale University School of Medicine, New Haven, Conn. (Deyama, Bang, Wohleb, Li, Kato, Gerhard, Dutheil, Dwyer, Taylor, Picciotto, Duman); Laboratory of Molecular Pharmacology, Institute of Medical, Pharmaceutical, and Health Sciences, Kanazawa University, Kanazawa, Japan (Deyama); Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati (Wohleb); Drug Development Research Laboratories, Sumitomo Dainippon Pharma, Suita, Japan (Kato).
Kanazawa University · JP
Funding
Cholinergic Contribution to Circuits Underlying DepressionR01MH077681 · NIMH · YALE UNIVERSITY · PI MINEUR, YANN SEBASTIEN, PICCIOTTO, MARINA R · 2006 to 2025
$7.0MRole of mTOR and Synaptogenesis in the Actions of Rapid-Acting AntidepressantsR01MH093897 · NIMH · YALE UNIVERSITY · PI DILEONE, RALPH J · 2011 to 2021
$5.0MAntidepressants: Signal Transduction and Gene ExpressionR37MH045481 · NIMH · YALE UNIVERSITY · PI DUMAN, RONALD S. · 2005 to 2014
$3.5MSynaptic mechanisms underlying the rapid antidepressant actions of scopolamineR01MH105910 · NIMH · YALE UNIVERSITY · PI PICCIOTTO, MARINA R · 2014 to 2018
$2.2MANTIDEPRESSANTS AND SIGNAL TRANSDUCTION IN BRAINR01MH045481 · NIMH · YALE UNIVERSITY · PI DUMAN, RONALD S. · 1995 to 2004
$1.3MNIMH NIH HHS R01 MH045481NIMH NIH HHS R01 MH077681NIMH NIH HHS R01 MH093897NIMH NIH HHS R01 MH105910NIMH NIH HHS R37 MH045481
Abstract
objectiveThe
methodsThe authors used a combination of approaches, including conditional, neuron-specific knockout of VEGF or its receptor, Flk-1; antibody neutralization; viral-mediated knockdown of Flk-1; and pharmacological inhibitors. Further in vitro and in vivo experiments were performed to examine whether neuronal VEGF signaling was required for the neurotrophic and synaptogenic actions of ketamine that underlie its behavioral actions.
resultsThe behavioral actions of systemic ketamine are blocked by forebrain excitatory neuron-specific deletion of either VEGF or Flk-1 or by intra-mPFC infusion of a VEGF neutralizing antibody. Moreover, intra-mPFC infusions of VEGF are sufficient to produce rapid ketamine-like behavioral actions, and these effects are blocked by neuron-specific Flk-1 deletion. The results also show that local knockdown of Flk-1 in mPFC excitatory neurons in adulthood blocks the behavioral effects of systemic ketamine. Moreover, inhibition of neuronal VEGF signaling blocks the neurotrophic and synaptogenic effects of ketamine.
conclusionsTogether, these findings indicate that neuronal VEGF-Flk-1 signaling in the mPFC plays an essential role in the antidepressant actions of ketamine.
Indexed as
AnimalsAntibodies, NeutralizingBehavior, AnimalExcitatory Amino Acid AntagonistsGene Knockdown TechniquesGene Knockout TechniquesIn Vitro TechniquesKetamineMiceNeuronsPrefrontal CortexQuinazolinesSignal TransductionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2Antibodies, NeutralizingExcitatory Amino Acid AntagonistsKetamineQuinazolinesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2ZM323881AntidepressantsMood Disorders-Unipolar
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