Article ID Journal Published Year Pages File Type
5628242 Epilepsy & Behavior 2017 5 Pages PDF
Abstract

•Seizures suppressed quantity and total duration of USVs.•Seizures altered the frequency distribution of call types utilized.•Seizures increased peak amplitude for five call types.•Seizures reduced mean call duration for short and two-syllable calls.•There were no changes in latency to first vocalization or inter-call intervals.

Early-life seizures are known to cause long-term deficits in social behavior, learning, and memory, however little is known regarding their acute impact. Ultrasonic vocalization (USV) recordings have been developed as a tool for investigating early communicative deficits in mice. Previous investigation from our lab found that postnatal day (PD) 10 seizures cause male-specific suppression of 50-kHz USVs on PD12 in 129 SvEvTac mouse pups. The present study extends these findings by spectrographic characterization of USVs following neonatal seizures.On PD10, male C57BL/6 pups were administered intraperitoneal injections of kainic acid or physiological saline. On PD12, isolation-induced recordings were captured using a broad-spectrum ultrasonic microphone. Status epilepticus significantly suppressed USV quantity (p = 0.001) and total duration (p < 0.05). Seizure pups also utilized fewer complex calls than controls (p < 0.05). There were no changes in call latency or inter-call intervals. Spectrographic analysis revealed increased peak amplitude for complex, downward, short, two-syllable, and upward calls, as well as reduced mean duration for short and two-syllable calls in seizure mice. This investigation provides the first known spectrographic characterization of USVs following early-life seizures. These findings also enhance evidence for USVs as an indicator of select communicative impairment.

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