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Abnormal social behaviors in mice lacking Fgf17
K Scearce-Levie1, E D Roberson, H Gerstein
1Gladstone Institute of Neurological Disease, San Francisco, CA 94158-2261, USA. kscearce-levie@gladstone.ucsf.edu
Genes, Brain, and Behavior
|October 3, 2007
Summary
Fibroblast growth factor 17 (Fgf17) is crucial for complex social behaviors in mice. Fgf17 deficiency impairs social interaction and vocalization, suggesting a role in neuropsychiatric disorders.
Area of Science:
- Neuroscience
- Developmental Biology
- Genetics
Background:
- Fibroblast growth factor (FGF) family members are vital signaling molecules for central nervous system development.
- Fibroblast growth factor 17 (Fgf17) plays a role in the regionalization of the rodent frontal cortex.
Purpose of the Study:
- To investigate the role of Fgf17 signaling in modulating mouse behavior during development and adulthood.
- To determine the impact of Fgf17 gene dosage on various behavioral phenotypes.
Main Methods:
- Studied mice with one or two deleted copies of the Fgf17 gene (Fgf17-deficient mice).
- Assessed a wide range of behaviors including physical growth, activity, anxiety, motor skills, learning, feeding, fear conditioning, aggression, olfactory exploration, and social interactions.
- Measured immediate-early gene Fos activation in the frontal cortex following social interaction tests.
Main Results:
- Fgf17-deficient mice exhibited no significant abnormalities in general physical growth, activity, anxiety, motor coordination, learning, feeding, fear conditioning, aggression, or olfactory exploration.
- Striking deficits were observed in specific social behaviors: Fgf17-deficient pups showed reduced vocalization when separated from their mother and siblings.
- Adult Fgf17-deficient males displayed decreased social interaction with novel females and reduced affiliative behaviors in opposite-sex pairs. Fos activation in the frontal cortex was lower in Fgf17-deficient mice after social exploration.
Conclusions:
- Fgf17 is essential for the execution of several complex social behaviors in mice.
- These findings suggest that disruptions in Fgf17 signaling could be implicated in the etiology of neuropsychiatric diseases characterized by social behavior deficits.
