Unlike the other mouse models of ASDs, individual neurexin and neuroligin mutants do not have many reported changes in dendritic spine density, which is somewhat surprising, given that neurexins (Graf et al., 2004) and neuroligins (Scheiffele et al., 2000) induce synapse formation in cultured cells in vitro and that knockdown of neuroligins in cultured neurons reduces spine density (Chih et al., 2005). This suggests that there may be functional redundancy in the different proteins that can compensate for one another during development in vivo. However, even mice lacking either all three α-Nrxn proteins (Missler et al., 2003) or Nlgn1, Nlgn2, and Nlgn3 (Varoqueaux et al., 2006) have normal synapse numbers, suggesting that these molecules may not be required for synapse formation at all. A more recent study showed that knockdown of Nlgn1 in vivo reduces synaptic density when neighboring neurons still express Nlgn1 (Kwon et al., 2012). Whereas mice lacking Nlgn2 have normal numbers of both excitatory and inhibitory synapses, they have decreased expression of VGAT, which represents an impairment in recruiting GABAergic synaptic vesicles to presynaptic terminals (Blundell et
