Activity-dependent validation of excitatory versus inhibitory synapses by neuroligin-1 versus neuroligin-2.

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Synaptic dysfunction in neurodevelopmental disorders associated with autism and intellectual disabilities. (2012, background): “The finding that Nlgn1 deficiency impairs N-methyl-D-aspartate (NMDA) receptor signaling, whereas Nlgn2 deficiency causes deficits in inhibitory synaptic transmission, is consistent with the localization of NLGN1 and 2 to excitatory and inhibitory synapses, respectively (Chubykin et al. 2007).”
Neuroligins and neurexins link synaptic function to cognitive disease (2008, background): “I suggest that these molecules are required for synapse function but not for synapse formation, that they affect trans-synaptic activation of synaptic transmission but are not essential for synaptic cohesion of the presynaptic and postsynaptic specializations, and that their dysfunction impairs the ”
The autistic neuron: troubled translation? (2008, background): “Recent evidence indicates that neuroligins stabilize new synapses and specify their functional properties, thereby regulating the balance of excitatory and inhibitory transmission (Chubykin et al., 2007) (see Essay by Walsh et al., page 396 of this issue).”