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Brain-specific Foxp1 deletion impairs neuronal development and causes autistic-like behaviour
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Brain-specific Foxp1 deletion impairs neuronal development and causes autistic-like behaviour
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Journal Article
Brain-specific Foxp1 deletion impairs neuronal development and causes autistic-like behaviour
2015
Overview
Neurodevelopmental disorders are multi-faceted and can lead to intellectual disability, autism spectrum disorder and language impairment. Mutations in the Forkhead box
FOXP1
gene have been linked to all these disorders, suggesting that it may play a central role in various cognitive and social processes. To understand the role of
Foxp1
in the context of neurodevelopment leading to alterations in cognition and behaviour, we generated mice with a brain-specific
Foxp1
deletion (
Nestin-Cre
Foxp1−/−
mice). The mutant mice were viable and allowed for the first time the analysis of pre- and postnatal neurodevelopmental phenotypes, which included a pronounced disruption of the developing striatum and more subtle alterations in the hippocampus. More detailed analysis in the CA1 region revealed abnormal neuronal morphogenesis that was associated with reduced excitability and an imbalance of excitatory to inhibitory input in CA1 hippocampal neurons in
Nestin-Cre
Foxp1−/−
mice.
Foxp1
ablation was also associated with various cognitive and social deficits, providing new insights into its behavioural importance.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/106
/ 13/51
/ 14
/ 14/19
/ 38
/ 38/39
/ 38/61
/ 38/90
/ 631/208
/ 64/60
/ 9/74
/ Analysis
/ Animals
/ Autism
/ Autistic Disorder - genetics
/ Brain - growth & development
/ Cell Proliferation - genetics
/ Developmental Disabilities - genetics
/ Developmental Disabilities - pathology
/ Forkhead Transcription Factors - deficiency
/ Forkhead Transcription Factors - genetics
/ Male
/ Medicine
/ Memory, Short-Term - physiology
/ Mice
/ Mutation
/ Original
/ Pervasive developmental disorders
/ Prepulse Inhibition - genetics
/ Repressor Proteins - deficiency
/ Repressor Proteins - genetics
