ArticleTranslational psychiatry2022
IGF-1 release in the medial prefrontal cortex mediates the rapid and sustained antidepressant-like actions of ketamine.
Article in Translational psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Modulation of early non-rapid eye movement slow wave activity by ketamine in treatment-resistant depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Trial
- Time-dependent effects of rapid-acting antidepressants in iPSC-derived neurons from treatment-resistant depression and healthy volunteers.Molecular psychiatry · 2026Article
- Associations of insulin-like growth factor-1 with gait vigor, symmetry, and stability metrics measured by wearable sensors in older adults.BMC geriatrics · 2026Article
- Time-Dependent Effects of Rapid-Acting Antidepressants in iPSC-Derived Neurons from Treatment-Resistant Depression and Healthy Volunteers.Research square · 2026Article
- Metabolic dysfunction and insulin resistance in depression: mechanisms, evidence, and therapeutic implications.Frontiers in psychiatry · 2026Review
- Review
- Ketamine and its enantiomers for depression: a bibliometric analysis from 2000 to 2023.European archives of psychiatry and clinical neuroscience · 2025Review
- The immunological perspective of major depressive disorder: unveiling the interactions between central and peripheral immune mechanisms.Journal of neuroinflammation · 2025Review
- Novel and emerging anesthetic drugs for the treatments of major depression: a comprehensive review of efficacy, mechanism, and outlook.Frontiers in psychiatry · 2025Review
- Individual differences in affect in response to physical activity.Frontiers in psychology · 2025Article
- Dual role of Lyz2-positive myeloid cells in traumatic brain injury: acute anti-inflammatory effects vs. chronic neurological deterioration.Frontiers in cellular neuroscience · 2025Article
- Ketamine and its two enantiomers in anesthesiology and psychiatry: A historical review and future directions.Journal of anesthesia and translational medicine · 2024Review
- Deconstructing depression by machine learning: the POKAL-PSY study.European archives of psychiatry and clinical neuroscience · 2024Article
- Repurposing Ketamine in the Therapy of Depression and Depression-Related Disorders: Recent Advances and Future Potential.Aging and disease · 2024Review
- Neuron-specific deletion of VEGF or its receptor Flk-1 occludes the antidepressant-like effects of desipramine and fluoxetine in mice.Neuropsychopharmacology reports · 2024Article
- Locus Coeruleus-Dorsolateral Septum Projections Modulate Depression-Like Behaviors via BDNF But Not Norepinephrine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- In Vivo Brain Microdialysis.Methods in molecular biology (Clifton, N.J.) · 2024Article
- The role of neurotrophic factors in novel, rapid psychiatric treatments.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Review
- Ketamine and the Disinhibition Hypothesis: Neurotrophic Factor-Mediated Treatment of Depression.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Bridging rapid and sustained antidepressant effects of ketamine.Trends in molecular medicine · 2023Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ketamine, an N-methyl-D-aspartate receptor antagonist, exerts rapid and sustained antidepressant actions. Preclinical studies demonstrated that the release of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor in the medial prefrontal cortex (mPFC) is essential for the antidepressant-like effects of ketamine. However, the role of other neurotrophic factors in the antidepressant-like effects of ketamine has not been fully investigated. Since the intra-mPFC infusion of insulin-like growth factor 1 (IGF-1) reportedly produced antidepressant-like effects, the present study examined the role of endogenous intra-mPFC IGF-1 signaling in the antidepressant-like actions of ketamine. In vivo microdialysis showed that ketamine (10 and 30 mg/kg) significantly increased extracellular IGF-1 levels in the mPFC of male C57BL/6J mice for at least 5 h. Infusion of an IGF-1 neutralizing antibody (nAb; 160 ng/side) into the mPFC 15 min before or 2 h after ketamine injection blocked the antidepressant-like effects of ketamine in three different behavioral paradigms (forced swim, female urine sniffing, and novelty-suppressed feeding tests were conducted 1, 3 and 4 days post-ketamine, respectively). The ketamine-like antidepressant-like actions of the intra-mPFC infusion of BDNF (100 ng/side) and IGF-1 (50 ng/side) respectively were not blocked by co-infused IGF-1 nAb and BDNF nAb (200 ng/side). Moreover, intra-mPFC infusion of IGF-1 nAb 2 h post-ketamine blocked the antidepressant-like effects of ketamine in a murine lipopolysaccharide (LPS)-induced depression model. Intra-mPFC IGF-1 infusion also produced antidepressant-like effects in the LPS-challenged mice via mechanistic target of rapamycin complex 1 activation. These results suggest that persistent release of IGF-1, independently of BDNF, in the mPFC is essential for the antidepressant-like actions of ketamine.
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