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

Josiah D ZoodsmaEmma J KeeganGabrielle R MoodyAshwin A Bhandiwad Amalia J Napoli Harold A Burgess Lonnie P Wollmuth Howard I Sirotkin

Published in: Molecular autism (2022)

We 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.

Keyphrases

autism spectrum disorder
healthcare
traumatic brain injury
intellectual disability
genome wide
current status
copy number
gene expression
protein kinase
genome wide analysis