A multitude of mice with mutations in the neurexins, neuroligins, and related genes have been generated to understand the roles of these cell adhesion molecules in normal development and in ASDs. Mice lacking either Nrxn1α (Etherton et al., 2009; Grayton et al., 2013) or Nrxn2α (Dachtler et al., 2014) show some ASD-like features. Additionally, mice with a subset of forebrain neurons overexpressing of a dominant-negative form of Nrxn1β missing its cytoplasmic tail display ASD-like behaviors (Rabaneda et al., 2014). Mice lacking Cntnap2 (Peñagarikano et al., 2011) or Cntnap4 (Karayannis et al., 2014) also have phenotypes which resemble ASD. Likewise, mice lacking Nlgn1 (Blundell et al., 2010), Nlgn2 (Blundell et al., 2009; Wöhr et al., 2013), Nlgn3 (Radyushkin et al., 2009; Rothwell et al., 2014), or Nlgn4 (Jamain et al., 2008; El-Kordi et al., 2013; Ju et al., 2014) all have ASD-like behaviors to various degrees. Mice with a knock-in mutation of NLGN3 (R451C) found in human populations have also been generated and recapitulate some ASD-like features (Tabuchi et al., 2007; Jaramillo et al., 2014; Rothwell et al., 2014).
