GRIN1 disorder is a neurodevelopmental disorder characterized by variation to the Grin1 gene; responsible for coding the obligatory GluN1 subunit of NMDA receptors. Individuals with GRIN1 disorder display developmental delay and speech is absent in almost half of patients. The Grin1Y647S/+ patient variant occurs within the M3 transmembrane domain of GluN1 and the patient displays limited speech consisting of 5-10 words. The Grin1Q536R/+ patient variant occurs in the S1 segment of the ligand binding domain of GluN1 and the patient has active speech with a relatively large vocabulary. We aimed to determine if Grin1Y647S/+ and Grin1Q536R/+ patient variant mouse models display developmental delay and communicative ability reminiscent of patient characteristics. Mice use ultrasonic vocalizations (USVs) to communicate with eachother and USVs emitted by pups during separation from their mother function to facilitate retrieval. USVs were collected in 10 litters at post-natal day (PND) 6, 8, 10 in response to maternal isolation. Weight, righting reflex and body measurements were collected at each PND to assess developmental delay. Both Grin1Y647S/+ and Grin1Q536R/+ did not differ from corresponding wildtype littermates in weight, body measurements and had intact righting reflex at all PNDs tested. At PND 6, Grin1Y647S/+ pups displayed significantly increased USVs and Grin1Q536R/+ displayed significantly decreased USVs compared to wildtype littermates. Grin1Q536R/+ displayed significantly decreased average change in frequency per USV, indicating reduced complexity. Therefore, Grin1 patient variant mouse models demonstrate alterations to post-natal USVs in response to maternal isolation. Future analyses will examine USVs in Grin1Y647S/+ and Grin1Q536R/+ at PND 8,10.