ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Loss of glutamatergic pyramidal neurons in frontal and temporal cortex resulting from attenuation of FGFR1 signaling is associated with spontaneous hyperactivity in mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 90 citations in OpenAlex.
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- Prenatal stress selectively enhances locomotor hyperactivity in male mice with embryonic loss ofFrontiers in psychiatry · 2026Article
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- Mapping brain asymmetry in health and disease through the ENIGMA consortium.Human brain mapping · 2022Review
- Enhanced FGFR3 activity in postmitotic principal neurons during brain development results in cortical dysplasia and axonal tract abnormality.Scientific reports · 2020Article
- No Alterations of Brain Structural Asymmetry in Major Depressive Disorder: An ENIGMA Consortium Analysis.The American journal of psychiatry · 2019Article
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- Fibroblast Growth Factors in Depression.Frontiers in pharmacology · 2019Review
- Loss of TrkB Signaling in Parvalbumin-Expressing Basket Cells Results in Network Activity Disruption and Abnormal Behavior.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- The Therapeutic Effect of the Chinese Herbal Medicine, Rehmanniae Radix Preparata, in Attention Deficit Hyperactivity DisorderEvidence-based complementary and alternative medicine : eCAM · 2018Review
- Recombinant human fibroblast growth factor-2 promotes nerve regeneration and functional recovery after mental nerve crush injury.Neural regeneration research · 2017Article
- Quantitative assessment of fibroblast growth factor receptor 1 expression in neurons and glia.PeerJ · 2017Article
- Deletion of fibroblast growth factor 22 (FGF22) causes a depression-like phenotype in adult mice.Behavioural brain research · 2016Article
- Molecular underpinnings of prefrontal cortex development in rodents provide insights into the etiology of neurodevelopmental disorders.Molecular psychiatry · 2015Review
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- Monoamine neurotransmitters and fibroblast growth factor-2 in the brains of rats with post-stroke depression.Experimental and therapeutic medicine · 2014Article
- Receptor tyrosine kinase (RTK) signalling in the control of neural stem and progenitor cell (NSPC) development.Molecular neurobiology · 2014Review
- The best-laid plans go oft awry: synaptogenic growth factor signaling in neuropsychiatric disease.Frontiers in synaptic neuroscience · 2014Review
- Article
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Authors and funding
7 authors at 5 institutions in 4 countries.
Funding
Abstract
Fibroblast growth factor receptor (FGFR) gene products (Fgfr1, Fgfr2, Fgfr3) are widely expressed by embryonic neural progenitor cells throughout the CNS, yet their functional role in cerebral cortical development is still unclear. To understand whether the FGF pathways play a role in cortical development, we attenuated FGFR signaling by expressing a tyrosine kinase domain-deficient Fgfr1 (tFgfr1) gene construct during embryonic brain development. Mice carrying the tFgfr1 transgene under the control of the Otx1 gene promoter have decreased thickness of the cerebral cortex in frontal and temporal areas because of decreased number of pyramidal neurons and disorganization of pyramidal cell dendritic architecture. These alterations may be, in part, attributable to decreased genesis of T-Brain-1-positive early glutamatergic neurons and, in part, to a failure to maintain radial glia fibers in medial prefrontal and temporal areas of the cortical plate. No changes were detected in cortical GABAergic interneurons, including Cajal-Retzius cells or in the basal ganglia. Behaviorally, tFgfr1 transgenic mice displayed spontaneous and persistent locomotor hyperactivity that apparently was not attributable to alterations in subcortical monoaminergic systems, because transgenic animals responded to both amphetamine and guanfacine, an alpha2A adrenergic receptor agonist. We conclude that FGF tyrosine kinase signaling may be required for the genesis and growth of pyramidal neurons in frontal and temporal cortical areas, and that alterations in cortical development attributable to disrupted FGF signaling are critical for the inhibitory regulation of motor behavior.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.