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 al., 2009). The Nlgn3R451C mice also have normal numbers of both excitatory and inhibitory synapses, but have increased expression of VGAT (Tabuchi et al., 2007). These mice have increased dendritic complexity in the stratum radiatum, decreased synaptic terminal size, fewer vesicles per terminal, and decreased spine size (Etherton et al., 2011a). Additionally, the Nlgn3R451C mice have increased dendritic spine turnover in pyramidal neurons in the anterior frontal cortex (Isshiki et al., 2014). Moreover, mice lacking Cntnap4 have increased width of synaptic clefts and decreased PSD length in GABAergic synapses (Karayannis et al., 2014).
