ArticleTranslational psychiatry2016
Genetic deletion of fibroblast growth factor 14 recapitulates phenotypic alterations underlying cognitive impairment associated with schizophrenia.
Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Maternal pesticide exposure disrupts local inhibitory circuits in the reward pathway.Environment international · 2026Article
- The Role of GABA Pathway Components in Pathogenesis of Neurodevelopmental Disorders.International journal of molecular sciences · 2025Review
- Loss of intracellular FGF14 (iFGF14) increases excitability of mature hippocampal pyramidal neurons.The Journal of general physiology · 2025Article
- Deletion of Fgf14 confers resilience to basal and stress-induced depressive-like behavior and reduces anxiety in mice.Translational psychiatry · 2025Article
- Environmental exposure to common pesticide induces synaptic deficit and social memory impairment driven by neurodevelopmental vulnerability of hippocampal parvalbumin interneurons.Journal of hazardous materials · 2025Article
- Pathology and Therapeutic Significance of Fibroblast Growth Factors.Targets (Basel) · 2025Article
- Transcriptomic sex differences in postmortem brain samples from patients with psychiatric disorders.Science translational medicine · 2024Article
- Blocking Site-Specific Cleavage of Human Tau Delays Progression of Disease-Related Phenotypes in Genetically Matched Tau-Transgenic Mice Modeling Frontotemporal Dementia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Pharmacologically Targeting the Fibroblast Growth Factor 14 Interaction Site on the Voltage-Gated NaInternational journal of molecular sciences · 2021Article
- Convergent genomic and pharmacological evidence of PI3K/GSK3 signaling alterations in neurons from schizophrenia patients.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- The Ketamine Antidepressant Story: New Insights.Molecules (Basel, Switzerland) · 2020Review
- Mapping of the FGF14:Nav1.6 complex interface reveals FLPK as a functionally active peptide modulating excitability.Physiological reports · 2020Article
- Broader phenotypic traits and widespread brain hypometabolism in spinocerebellar ataxia 27.Journal of internal medicine · 2020Article
- The role of miR-711 in cardiac cells in response to oxidative stress and its biogenesis: a study on H9C2 cells.Cellular & molecular biology letters · 2020Article
- High-throughput screening against protein:protein interaction interfaces reveals anti-cancer therapeutics as potent modulators of the voltage-gated NaScientific reports · 2019Article
- Factors other than hTau overexpression that contribute to tauopathy-like phenotype in rTg4510 mice.Nature communications · 2019Article
- Sex-Specific Proteomic Changes Induced by Genetic Deletion of Fibroblast Growth Factor 14 (FGF14), a Regulator of Neuronal Ion Channels.Proteomes · 2019Article
- Changes in the Fluorescence Tracking of NaV1.6 Protein Expression in a BTBR T+Itpr3tf/J Autistic Mouse Model.Neural plasticity · 2019Article
- Emerging roles of Fgf14 in behavioral control.Behavioural brain research · 2019Article
- Maternal inhalation of carbon black nanoparticles induces neurodevelopmental changes in mouse offspring.Particle and fibre toxicology · 2018Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 3 countries.
Funding
Abstract
Cognitive processing is highly dependent on the functional integrity of gamma-amino-butyric acid (GABA) interneurons in the brain. These cells regulate excitability and synaptic plasticity of principal neurons balancing the excitatory/inhibitory tone of cortical networks. Reduced function of parvalbumin (PV) interneurons and disruption of GABAergic synapses in the cortical circuitry result in desynchronized network activity associated with cognitive impairment across many psychiatric disorders, including schizophrenia. However, the mechanisms underlying these complex phenotypes are still poorly understood. Here we show that in animal models, genetic deletion of fibroblast growth factor 14 (Fgf14), a regulator of neuronal excitability and synaptic transmission, leads to loss of PV interneurons in the CA1 hippocampal region, a critical area for cognitive function. Strikingly, this cellular phenotype associates with decreased expression of glutamic acid decarboxylase 67 (GAD67) and vesicular GABA transporter (VGAT) and also coincides with disrupted CA1 inhibitory circuitry, reduced in vivo gamma frequency oscillations and impaired working memory. Bioinformatics analysis of schizophrenia transcriptomics revealed functional co-clustering of FGF14 and genes enriched within the GABAergic pathway along with correlatively decreased expression of FGF14, PVALB, GAD67 and VGAT in the disease context. These results indicate that Fgf14(-/-) mice recapitulate salient molecular, cellular, functional and behavioral features associated with human cognitive impairment, and FGF14 loss of function might be associated with the biology of complex brain disorders such as schizophrenia.
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