ArticleThe international journal of neuropsychopharmacology2014
Fluoxetine regulates neurogenesis in vitro through modulation of GSK-3β/β-catenin signaling.
Article in The international journal of neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Neuronal Stem Cell and Drug Interactions: A Systematic Review and Meta-Analysis: Concise Review.Stem cells translational medicine · 2019Pooled it
- Fluoxetine Repurposing Mitigates Alzheimer's Disease Pathology via the GSK3β-CREB-ADAM10 Axis.International journal of molecular sciences · 2026Article
- Network pharmacology of cellular targets in major depressive disorder and differential mechanisms of fluoxetine, ketamine and esketamine.Computational and structural biotechnology journal · 2026Article
- Across Barriers: Blood-Brain and Gut Barrier Signaling in Psychiatric Disorders.Journal of neurochemistry · 2025Review
- Repurposing Sigma-1 Receptor-Targeting Drugs for Therapeutic Advances in Neurodegenerative Disorders.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Assessing the Neurodevelopmental Impact of Fluoxetine, Citalopram, and Paroxetine on Neural Stem Cell-Derived Neurons.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Fluoxetine Rescues Excessive Myelin Formation and Psychological Behaviors in a Murine PTSD Model.Neuroscience bulletin · 2024Article
- Damage mechanism and therapy progress of the blood-brain barrier after ischemic stroke.Cell & bioscience · 2023Review
- Transcriptional Regulation of the Human 5-HT1A Receptor Gene by Lithium: Role of Deaf1 and GSK3β.International journal of molecular sciences · 2023Article
- Article
- Olanzapine add-on treatment promotes neuronal differentiation of neural stem cells compared with fluoxetine alone.Bioscience reports · 2022Article
- Fluoxetine increases astrocytic glucose uptake and glycolysis in corticosterone-induced depression through restricting GR-TXNIP-GLUT1 Pathway.Frontiers in pharmacology · 2022Article
- The Gender-Specific Interaction ofOxidative medicine and cellular longevity · 2022Article
- Effects of the Selective Serotonin Reuptake Inhibitor Fluoxetine on Developing Neural Circuits in a Model of the Human Fetal Cortex.International journal of molecular sciences · 2021Article
- Fluoxetine regulates eEF2 activity (phosphorylation) via HDAC1 inhibitory mechanism in an LPS-induced mouse model of depression.Journal of neuroinflammation · 2021Article
- Opportunities for multiscale computational modelling of serotonergic drug effects in Alzheimer's disease.Neuropharmacology · 2020Review
- Glycogen synthase kinase-3 signaling in cellular and behavioral responses to psychostimulant drugs.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Structural Changes in Hippocampal Subfields in Patients with Continuous Remission of Drug-Naive Major Depressive Disorder.International journal of molecular sciences · 2020Article
- The selective GSK3 inhibitor, SAR502250, displays neuroprotective activity and attenuates behavioral impairments in models of neuropsychiatric symptoms of Alzheimer's disease in rodents.Scientific reports · 2019Article
- Complex Combination Pharmacotherapy for Bipolar Disorder: Knowing When Less Is More or More Is Better.Focus (American Psychiatric Publishing) · 2019Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIt is generally accepted that chronic treatment with antidepressants increases hippocampal neurogenesis, but the molecular mechanisms underlying their effects are unknown. Recently, glycogen synthase kinase-3 beta (GSK-3β)/β-catenin signaling was shown to be involved in the mechanism of how antidepressants might influence hippocampal neurogenesis.
methodsThe aim of this study was to determine whether GSK-3β/β-catenin signaling is involved in the alteration of neurogenesis as a result of treatment with fluoxetine, a selective serotonin reuptake inhibitor. The mechanisms involved in fluoxetine's regulation of GSK-3β/β-catenin signaling pathway were also examined.
resultsOur results demonstrated that fluoxetine increased the proliferation of embryonic neural precursor cells (NPCs) by up-regulating the phosphorylation of Ser9 on GSK-3β and increasing the level of nuclear β-catenin. The overexpression of a stabilized β-catenin protein (ΔN89 β-catenin) significantly increased NPC proliferation, while inhibition of β-catenin expression in NPCs led to a significant decrease in the proliferation and reduced the proliferative effects induced by fluoxetine. The effects of fluoxetine-induced up-regulation of both phosphorylation of Ser9 on GSK-3β and nuclear β-catenin were significantly prevented by the 5-hydroxytryptamine-1A (5-HT1A) receptor antagonist WAY-100635.
conclusionsThe results demonstrate that fluoxetine may increase neurogenesis via the GSK-3β/β-catenin signaling pathway that links postsynaptic 5-HT1A receptor activation.
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