Loss-of-function mutations in the synaptic protein neurexin1α (NRXN1α) are associated with several neurodevelopmental disorders, including autism spectrum disorder (ASD), schizophrenia, and attentiondeficit hyperactivity disorder (ADHD), and many of these disorders are defined by core deficits in social cognition. Mouse models of Nrxn1α deficiency are not amenable to studying aspects of social cognition because, in general, mice do not engage in complex social interactions such as social play or prosocial helping behaviors. Rats, on the contrary, engage in these complex, well-characterized social behaviors. Using the Nrxn1 tm1Sage Sprague Dawley rat, we tested a range of cognitive and social behaviors in juveniles with haplo-or biallelic Nrxn1α mutation. We found a deficit in ultrasonic vocalizations (USVs) of male and female neonatal rats with Nrxn1α deficiency. A male-specific deficit in social play was observed in Nrxn1αdeficient juveniles, although sociability and social discrimination were unaltered. Nurturing behavior induced by exposure to pups was enhanced in male and female juveniles with biallelic Nrxn1α mutation. Performance in tasks of prosocial helping behavior and food retrieval indicated severe deficits in learning and cognition in juveniles with biallelic Nrxn1α mutation, and a less severe deficit in haploinsufficient rats, although Pavlovian learning was altered only in haploinsufficient males. We also observed a male-specific increase in mobility and object investigation in juveniles with complete Nrxn1α deficiency. Together, these observations more fully characterize the Nrxn1 tm1Sage Sprague Dawley rat as a model for Nrxn1α-related neurodevelopmental disorders, and support a rationale for the juvenile rat as a more appropriate model for disorders that involve core deficits in complex social behaviors.