Humans and other animals learn many of their complex and socially-oriented behaviors by imitating more experienced individuals in their environment. For example, development of spoken language is rooted in a child’s ability to imitate the speech patterns of their parent(s) and other adults. Disruptions of behaviors that rely on social experience, like social skills, speech and language, can be an important early indicator of autism spectrum disorders (ASDs). Although genetic manipulations of ASD risk genes can now be applied in many animal models, most model organisms do not robustly or naturally imitate behaviors, making it challenging to study how high-risk ASD genes impact learning of socially transmitted behaviors.

To address these experimental limitations, Todd Roberts and his colleagues are using songbirds as a new model system to study the role of high-risk ASD genes. Songbirds, like the zebra finch, learn their song via imitation, continually transmitting this behavior from one generation to the next. This provides an opportunity to examine how ASD risk genes impact the neural circuits involved in learning from social experience and in sensorimotor imitation of observed behaviors.

Roberts’ team is currently dissecting the role of the high-risk ASD gene FOXP1 (forkhead-box protein 1) in pallial circuits important for the social transmission of vocal behavior between adult and juvenile songbirds. FOXP1 is among the top five most significant ASD risk genes, and its haploinsufficiency causes specific language impairment and intellectual disability. FoxP1 is expressed in many of the same areas of the pallium and basal ganglia in both mammals and zebra finches, and it is also expressed in forebrain regions known to be important for song learning.

Using reversible genetic knockdown of FoxP1 combined with electrophysiological and in vivo two-photon imaging approaches, their research is revealing that FoxP1 plays a critical role in the ability of young birds to form memories of their vocal model¹. Current studies are aimed at understanding if circuit deficits associated with disrupted expression of FoxP1 can be rescued to re-enable learning. Future studies will look at the role of other high-risk ASD genes using the approaches developed here.