Neonatal loss of FGFR2 in astroglial cells affects locomotion, sociability, working memory, and glia-neuron interactions in mice

Hanna E. Stevens; Soraya Scuderi; Sarah C. Collica; Simone Tomasi; Tamas L. Horvath; Flora M. Vaccarino

doi:10.1038/s41398-023-02372-y

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Neonatal loss of FGFR2 in astroglial cells affects locomotion, sociability, working memory, and glia-neuron interactions in mice

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Neonatal loss of FGFR2 in astroglial cells affects locomotion, sociability, working memory, and glia-neuron interactions in mice

Hanna E. Stevens, Soraya Scuderi, Sarah C. Collica, Simone Tomasi, Tamas L. Horvath and Flora M. Vaccarino

Translational psychiatry, Vol.13(1), pp.89-89

03/11/2023

DOI: 10.1038/s41398-023-02372-y

PMCID: PMC10008554

PMID: 36906620

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Abstract

Fibroblast growth factor receptor 2 (FGFR2) is almost exclusively expressed in glial cells in postnatal mouse brain, but its impact in glia for brain behavioral functioning is poorly understood. We compared behavioral effects from FGFR2 loss in both neurons and astroglial cells and from FGFR2 loss in astroglial cells by using either the pluripotent progenitor-driven hGFAP-cre or the tamoxifen-inducible astrocyte-driven GFAP-creER T2 in Fgfr2 floxed mice. When FGFR2 was eliminated in embryonic pluripotent precursors or in early postnatal astroglia, mice were hyperactive, and had small changes in working memory, sociability, and anxiety-like behavior. In contrast, FGFR2 loss in astrocytes starting at 8 weeks of age resulted only in reduced anxiety-like behavior. Therefore, early postnatal loss of FGFR2 in astroglia is critical for broad behavioral dysregulation. Neurobiological assessments demonstrated that astrocyte-neuron membrane contact was reduced and glial glutamine synthetase expression increased only by early postnatal FGFR2 loss. We conclude that altered astroglial cell function dependent on FGFR2 in the early postnatal period may result in impaired synaptic development and behavioral regulation, modeling childhood behavioral deficits like attention deficit hyperactivity disorder (ADHD).

ADHD

Molecular neuroscience

Details

Title: Subtitle: Neonatal loss of FGFR2 in astroglial cells affects locomotion, sociability, working memory, and glia-neuron interactions in mice
Creators: Hanna E. Stevens - Yale University
Soraya Scuderi - New Haven, CT 06520 USA
Sarah C. Collica - New Haven, CT 06520 USA
Simone Tomasi - New Haven, CT 06520 USA
Tamas L. Horvath - New Haven, CT 06520 USA New Haven, CT 06520 USA
Flora M. Vaccarino - New Haven, CT 06520 USA New Haven, CT 06520 USA
Resource Type: Journal article
Publication Details: Translational psychiatry, Vol.13(1), pp.89-89
DOI: 10.1038/s41398-023-02372-y
PMID: 36906620
PMCID: PMC10008554
NLM abbreviation: Transl Psychiatry
eISSN: 2158-3188
Publisher: Nature Publishing Group UK
Grant note: ; R01 MH067715 / ; Junior Research Program of Excellence / ;
Language: English
Date published: 03/11/2023
Academic Unit: Psychiatry; Iowa Neuroscience Institute
Record Identifier: 9984378330202771

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