Journal article
Deletion of fibroblast growth factor 22 (FGF22) causes a depression-like phenotype in adult mice
Behavioural brain research, Vol.307, pp.11-17
07/01/2016
DOI: 10.1016/j.bbr.2016.03.047
PMCID: PMC4853240
PMID: 27036645
Abstract
•Mice lacking fibroblast growth factor 22 (FGF22KO) have depressive-like behaviors.•FGF22KO mice have normal motor, exploratory, and social behaviors.•Fibroblast growth factor 22 plays specific roles in affective behaviors.
Specific growth factors induce formation and differentiation of excitatory and inhibitory synapses, and are essential for brain development and function. Fibroblast growth factor 22 (FGF22) is important for specifying excitatory synapses during development, including in the hippocampus. Mice with a genetic deletion of FGF22 (FGF22KO) during development subsequently have fewer hippocampal excitatory synapses in adulthood. As a result, FGF22KO mice are resistant to epileptic seizure induction. In addition to playing a key role in learning, the hippocampus is known to mediate mood and anxiety. Here, we explored whether loss of FGF22 alters affective, anxiety or social cognitive behaviors in mice. We found that relative to control mice, FGF22KO mice display longer duration of floating and decreased latency to float in the forced swim test, increased immobility in the tail suspension test, and decreased preference for sucrose in the sucrose preference test, which are all suggestive of a depressive-like phenotype. No differences were observed between control and FGF22KO mice in other behavioral assays, including motor, anxiety, or social cognitive tests. These results suggest a novel role for FGF22 specifically in affective behaviors.
Details
- Title: Subtitle
- Deletion of fibroblast growth factor 22 (FGF22) causes a depression-like phenotype in adult mice
- Creators
- Aislinn J Williams - Molecular and Behavioral Neuroscience Institute and Department of Psychiatry, University of Michigan, Ann Arbor, MI, United StatesPatricia Yee - Boston Children’s Hospital and Harvard Medical School, Boston, MA, United StatesMitchell C Smith - Molecular and Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, MI, United StatesGeoffrey G Murphy - Molecular and Behavioral Neuroscience Institute and Department of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI, United StatesHisashi Umemori - Boston Children’s Hospital and Harvard Medical School, Boston, MA, United States
- Resource Type
- Journal article
- Publication Details
- Behavioural brain research, Vol.307, pp.11-17
- DOI
- 10.1016/j.bbr.2016.03.047
- PMID
- 27036645
- PMCID
- PMC4853240
- NLM abbreviation
- Behav Brain Res
- ISSN
- 0166-4328
- eISSN
- 1872-7549
- Publisher
- Elsevier BV
- Language
- English
- Date published
- 07/01/2016
- Academic Unit
- Psychiatry; Iowa Neuroscience Institute
- Record Identifier
- 9984065839302771
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