Social and Vocal Behaviors of a Novel ASD Mouse Model

Background:   Autism, or the more broadly defined autism spectrum disorders (ASDs), is multifaceted and likely due to a combination of genetic and environmental interactions. Two of the core deficits in ASD are abnormal social interactions and impairments in the ability to use language. Several genetically engineered mice have been developed in order to experimentally address these behavioral characteristics.  Because disrupted communication is a core feature of ASD and language is a human-specific feature, it is particularly challenging to study this aspect in non-human animal models.  Previous studies have uncovered ASD patients with mutations in FOXP1.  FOXP1 is a transcription factor and a member of the FOXP family of genes. A closely related family member, FOXP2 has been linked to language impairment in humans and alterations in ultrasonic vocalizations in mice. 

Objectives:   Due to the direct association of FOXP2 to language and vocalization and its close association to FOXP1, we explored the potential connection of FOXP1 to vocalizations.  Thus, we ascertained whether mutation of Foxp1 in rodents would have an impact on social and vocal behaviors. 

Methods:   We conducted a wide array of behavioral tests including open field, social preference, and ultrasonic vocalizations among others.

Results:   We observed a distinctive difference in the ability of the Foxp1 mutant mice to perform at comparable levels to wild-type litter mates on assays testing social interaction and learning. In addition, analysis of pup vocalizations revealed distinct differences in the developmental pattern of the Foxp1 mutant mice versus wild-type litter mates. 

Conclusions:   A preliminary interpretation of these differences suggests the vocalization repertoire of the Foxp1 mutants is delayed.  This delay in the production of maternal separation calls might be an early indicator of abnormal social behaviors and learning impairments caused by altered levels of Foxp1.  Together, these data suggest that Foxp1 mutant mice may be a novel model system for the study of ASD pathophysiology.