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}.