Neuroligins (Nlgns) are a family of postsynaptic transmembrane cell adhesion proteins that play a crucial role in excitation and inhibition balance through their regulation of GABAergic and glutamatergic signaling. 5 Neuroligin family members have been identified in humans: NL1, NL2, NL3, NL4X, and NL4Y.  NL 1-3 have close homologs in mice. Neurogilins have been identified in rodents, chicken, Drosophila, and C. elegans. 

Neuroligin structure contains extracellular acetylcholinesterase like domain that lacks esterase activity, a single transmembrane domain, and a short cytoplasmic tail containing a type I PDZ-domain-binding motif that functions in intracellular protein-protein interactions and signaling processes. Neuroligins and neurexins are known to interact with each other^1,2.

Neuroligin 3 is encoded by the Nlgn3 gene and seems to be ubiquitously expressed in the brain. Despite this fact, Neuroligin 3 functions in synaptic transmission appears to be region specific, affecting the somatosensory cortex and the hippocampus differently².

In humans, a missense mutation in Nlgn3 (Nlgn3^R451C) causing reduced synaptic expression of the protein is associated with non-syndromic autism spectrum disorders. In addition, Nlgn3 deletion shows impaired social interaction and vocal communication in rodent models.