1.1. Neurexins and neuroligins
Due to their critical role in synapse formation and maintenance, mutations impacting presynaptic neurexins and postsynaptic neuroligins have the potential to cause numerous structural and functional changes in the hippocampal circuit. In the scope of ASD models, one member of neuroligin family, neuroligin 3 (NGL3), expressed postsynaptically at both inhibitory and excitatory synapses, has been implicated both as a non-syndromic gene in ASD patients \cite{RN24,RN25} and a key regulator of E/I balance in the hippocampus of mice \cite{RN26,RN27}. Neuroligin-4 (Nlgn4) loss-of-function mutations are associated with monogenic heritable ASD and although there is debate about the validity of the mouse homolog \cite{RN29,RN28}, Ngln4-KO mice demonstrate alterations in both synaptic and behavior. A third gene in this family that has become an increasing focus of ASD studies in model animals is Contactin Associated Protein 2 (Cntnap2), a member of the neurexin family in which multiple mutations linked to ASD or ASD-like disorders have been identified \cite{RN30}.