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Garrett, L. ; Becker, L. ; Rozman, J. ; Puk, O. ; Stöger, T. ; Yildirim, A.Ö. ; Bohla, A. ; Eickelberg, O. ; Hans, W. ; Prehn, C. ; Adamski, J. ; Klopstock, T.* ; Rácz, I.* ; Zimmer, A.* ; Klingenspor, M.* ; Fuchs, H. ; Gailus-Durner, V. ; Wurst, W. ; Hrabě de Angelis, M. ; Graw, J. ; Hölter, S.M.

Fgf9Y162C mutation alters information processing and social memory in mice.

Mol. Neurobiol. 55, 4580–4595 (2017)
Forschungsdaten Zum Artikel DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
In neuropsychiatric diseases, such as major depression and anxiety, pathogenic vulnerability is partially dictated by a genetic predisposition. The search continues to define this genetic susceptibility and establish new genetic elements as potential therapeutic targets. The fibroblast growth factors (FGFs) could be interesting in this regard. This family of signaling molecules plays important roles in development while also functioning within the adult. This includes effects on aspects of brain function such as neurogenesis and synapse formation. Of this family, Fgf9 is expressed in the adult brain, but its functional role is less well defined. In this study, we examined the role of Fgf9 in different brain functions by analyzing the behavior of Fgf9 (Y162C) mutant mice, an Fgf9 allele without the confounding systemic effects of other Fgf9 genetic models. Here, we show that this mutation caused altered locomotor and exploratory reactivity to novel, mildly stressful environments. In addition, mutants showed heightened acoustic startle reactivity as well as impaired social discrimination memory. Notably, there was a substantial decrease in the level of adult olfactory bulb neurogenesis with no difference in hippocampal neurogenesis. Collectively, our findings indicate a role for the Fgf9 (Y162C) mutation in information processing and perception of aversive situations as well as in social memory. Thus, genetic alterations in Fgf9 could increase vulnerability to developing neuropsychiatric disease, and we propose the Fgf9 (Y162C) mutant mice as a valuable tool to study the predictive etiological aspects.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Fibroblast Growth Factor 9 ; Neuropsychiatric Disease ; Mice ; Brain ; Adult Neurogenesis
Sprache englisch
Veröffentlichungsjahr 2017
HGF-Berichtsjahr 2017
ISSN (print) / ISBN 0893-7648
e-ISSN 1559-1182
Zeitschrift Molecular Neurobiology
Quellenangaben Band: 55, Heft: 6, Seiten: 4580–4595 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort Clifton, NJ
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Developmental Genetics (IDG)
Institute of Experimental Genetics (IEG)
Institute of Lung Health and Immunity (LHI)
Molekulare Endokrinologie und Metabolismus (MEM)
POF Topic(s) 30204 - Cell Programming and Repair
30201 - Metabolic Health
90000 - German Center for Diabetes Research
30202 - Environmental Health
Forschungsfeld(er) Genetics and Epidemiology
Lung Research
PSP-Element(e) G-500500-001
G-500600-001
G-501900-022
G-505000-007
G-501600-001
G-505600-001
DOI 10.1007/s12035-017-0659-3
WOS ID WOS:000431991500005
Scopus ID 85022202022
PubMed ID 28695538
Permalink http://rdcu.be/t5qA
Erfassungsdatum 2017-07-12
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