Ultrasonic Vocalization Behavior in -Fmr1- Knockout Mice Following Early Life Seizures
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Fragile X Syndrome (FXS) is a genetic disorder caused by an expansion mutation of the CGG triplet in the –fmr-1 gene on the X chromosome. This disorder is characterized by hyperactivity, increased anxiety, repetitive-stereotyped behaviors, and impaired language development. Many children diagnosed with FXS also experience seizures during their lifetime. Previous studies estimate the comorbidity between FXS and epilepsy to be approximately 20%. However, the underlying etiology of this relationship is not fully understood. Ultrasonic vocalizations (UVs) are one tool that may be used to measure early behavioral changes in mice pups. In the present study we used neonatal UVs to analyze early communicative behaviors in a mouse model of FXS, both with and without early life seizures. On postnatal day (PD) 10, we administered 2.5 mg/kg of kainic acid via intraperitoneal injections to male FXS knockout (KO) and wild type (WT) mice to induce continuous seizures (status epilepticus). On PD 12, pups from all groups were temporarily isolated from their dam and ultrasonic vocalizations were recorded. We found a several alterations in number and duration of certain type of calls emitted in the KO seizure mice when compared to the WT seizure mice. In particular there were differences in the chevron, complex, composite, short, and downward types of vocalizations. There was an overall decrease in the number of calls made by the KO seizure group, p<.05. Our results provide support that early-life seizures and Fmr1 knockout can impact the communication aspect of behavior in mice during early development.