Disrupted Developmental Trajectory of Ultrasonic Vocalizations in a Rat Model of Fragile X Syndrome
Communication deficits are a defining feature of autism spectrum disorder (ASD) and among the earliest detectable markers of atypical neurodevelopment. Yet how specific genetic ASD risk factors shape the developmental trajectory of vocal communication remains poorly understood. Fragile X syndrome (FXS) is the most common inherited cause of ASD, resulting from the transcriptional silencing of the…
Ultrasonic vocalizations (USVs) are a key aspect of communication in rats and serve as a model for studying early vocal development in Fragile X syndrome (FXS), a genetic cause of autism spectrum disorder (ASD). FXS is caused by the silencing of the FMR1 gene, leading to impaired language development and atypical vocal communication in affected individuals.
To investigate how the FMR1 mutation influences USVs in rats, researchers compared the vocalizations of Fmr1 knockout (KO) and wildtype (WT) rats during maternal isolation from postnatal days 3 to 21. They discovered that Fmr1 KO rat pups produced fewer calls during the critical period of isolation-induced calling (p6-p10) compared to their WT littermates.
While the acoustic structure and temporal organization of the USVs remained largely unchanged in the KO group, the network analysis revealed a significant delay and alteration in the developmental trajectory of syntactic complexity. WT pups showed a progressive increase in syntactic complexity from day p3 to p10, whereas this developmental progression was disrupted in Fmr1 KO pups.
These findings indicate that the FMR1 mutation not only affects vocal production in rats but also impairs the developmental expansion of syntactic flexibility, making USV syntax a valuable indicator of atypical communicative development in FXS models.
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