The hypothesis that an alteration of synaptic functions could lead to autism spectrum disorders (ASD) was recently confirmed by the identification of mutations in synaptic proteins such as neuroligins, neurexins, Shank and contactins. Following these genetic studies, animal models were developed to better characterise the role of susceptibility genes in ASD. Knockout (KO) mice for the NLGN3 and NLGN4 genes showed a reduced interest in social interactions and a lower call rate than wild type mice. To further understand how mutations in the various genes implicated in ASD contributed to symptoms in the social, communicative or stereotyped behaviours, we compared the development of wild type mice and KO littermates for the NLGN4 and CNTN6 genes separately. We recorded pup isolation calls and examined developmental milestones every two days between P2 and P12. We expected deficits in acoustic communication to emerge in young pups, while their physical development should remain similar between KOs and wild types. Preliminary analyses of our data did not reveal any clear evidence of deficits in motor coordination and geotaxis perception. In contrast, NLGN4 KO mice tended to utter isolation calls at a lower rate than their wild type littermates. Further investigations will concentrate on the social and vocal behaviour of juvenile and adult littermates, and examine possible environmental effects on these phenotypes. Screening the behavioural phenotypes of further mutants should allow us to map the deficits related to each mutation over the long term.