In addition to the study that reported ASD-like behaviors in mice overexpressing a dominant-negative form of Nrxn1β in a subset of excitatory forebrain neurons (CaMKIIα-tTa; Rabaneda et al., 2014), another study involved various conditional knockouts of Nlgn3 to determine the cell types and brain regions involved in the behaviors (Rothwell et al., 2014). The authors of the latter study found that depletion of Nlgn3 in the D1-MSNs (D1-Cre) of the nucleus accumbens (localized injection of AAV-Cre) was sufficient to drive repetitive motor routines on the rotarod test, whereas depletion of Nlgn3 in D2-MSNs (A2a-Cre) or in the dorsal striatum (localized injection of AAV-Cre) was not (Rothwell et al., 2014). Moreover, depletion of Nlgn3 in Purkinje cells (P7-Cre) or parvalbumin-positive interneurons (PV-Cre) did not affect motor performance, but increased and decreased activity in the open field, respectively (Rothwell et al., 2014).
