Disruption of grin2B, an ASD-associated gene, produces social deficits in zebrafish

ConclusionsWe demonstrate that zebrafish completely lacking the GluN2B subunit of the NMDAR, unlike rodent models, are viable into adulthood. Notably, they exhibit a highly specific deficit in social behavior. As such, this zebrafish model affords a unique opportunity to study the roles of GluN2B in ASD etiologies and establish a disease-relevant in vivo model for future studies.
Source: Molecular Autism - Category: Molecular Biology Source Type: research