The neuroligin (NL) gene family has been well characterized in neurons by virtue of its role as a synaptic cell adhesion molecule, and because mutations in the gene have been associated with Autism Spectrum Disorder (ASD). However much less is known about its role in the glial cell population, where one of the subtypes, neuroligin 3, is expressed. The work presented here investigates NL’s role in oligodendrocytes (OLs), a subtype of glial cells responsible for the myelination in the central nervous system. This was accomplished by first determining NL’s presence in this cell type in hippocampal dissociated cultures by immunocytochemistry and in situ hybridization. It was found that by interfering with the interaction of NL and its pre-synaptic partner neurexin (NX), the developmental profile of OL cells was delayed. Conversely, enhancing the interaction accelerated the developmental profile. Evidence is also presented that glutamate receptors are potentially spatially localized to the contact points between oligodendrocytes and axons in response to the interaction between NL and NX. As mutations in NL have been linked to autism, this provides a new potential mechanism by which the cognitive deficits observed could occur.