Although changes in cellular and spine morphology in neurexin and neuroligin mouse models of ASD are somewhat minor, synaptic function is drastically altered. Deletion of Nrxn1α leads to reduced mEPSC frequency and decreased excitatory synaptic strength in the CA1 region of the hippocampus (Etherton et al., 2009). Mice with the dominant-negative form of Nrxn1β have decreased mEPSC frequency and mIPSC frequncy in L5/6 pyramidal neurons from the somatosensory cortex (Rabaneda et al., 2014). Mice lacking Cntnap4 have increased dopamine signaling through a presynaptic mechanism in the nucleus accumbens but fewer, smaller, and slower sIPSCs in PV-positive cells of the somatosensory cortex (Karayannis et al., 2014). Deletion of Nlgn1 results in a decrease in AMPAR EPSCs, NMDA EPSCs, and an increase in the AMPA/NMDA current ratio in the CA1 region of the hippocampus (Budreck et al., 2013) as well as impaired LTP at thalamic inputs to the amygdala (Jung et al., 2010). Impaired LTP has also been observed the hippocampi of Nlgn1 mutants in vitro (Blundell et al., 2010) and in vivo (Jedlicka et al., 2015). Mice lacking Nlgn4 have decreased
