Characterization of Social Behaviors Reveals a Novel Ultrasonic Vocalization Deficit in Fragile X Syndrome Mouse Models of Mental Retardation
The goal of this study was to investigate the social vocalizations of mouse models of Fragile X Syndrome (FXS), the most common inherited mental retardation in people. Those with FXS also have high rates of autistic symptoms. Both mental retardation and autism often create significant problems in verbal communication. It has been shown that mice produce ultrasonic vocalizations (USVs) during social interactions, but the effects of FX mutations on USV production has not been previously reported. In these experiments, it was found that Fragile X knockout (ko) mice displayed a pronounced deficit in total duration of USVs compared to wild-type (wt) mice, even though other measures of social interaction did not show a difference between the two. Knockout mice having at least one copy of a human FMR1 transgene were as vocal as non-transgenic wt mice, confirming the significance of Fmr1 on vocalization. It had been previously shown that seizures were elevated in FX mice, and that the seizures could be suppressed by specific glycogen synthase kinase 3 (GSK3) antagonists as well as lithium. Here it was found that lithium present in the diet increased vocalizations dramatically, suggesting that GSK3 may interact with Fmr1 in a common vocalization pathway.
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