Related Experiment Video
Updated: Mar 18, 2026
Determining Ultrasonic Vocalization Preferences in Mice using a Two-choice Playback Test
Published on: September 3, 2015
The effect of early life status epilepticus on ultrasonic vocalizations in mice
Conner D Reynolds1, Gregory Smith2, Taylor Jefferson1
1Department of Psychology and Neuroscience, Baylor University, Waco, Texas, U.S.A.
Insights
Early life seizures in mice significantly reduced ultrasonic vocalizations, particularly in males. This disruption in communication behavior was linked to changes in key neural signaling pathways.
Area of Science:
- Neuroscience
- Developmental Biology
- Behavioral Science
Background:
- Infant crying is a fundamental communication method for neonates, signaling needs to caregivers.
- Early life vocalizations in rodents are being explored as potential markers for neurodevelopmental disorders.
- The impact of neonatal seizures on vocalization behavior and underlying neural mechanisms remains understudied.
Purpose of the Study:
- To investigate the effects of a single kainate-induced seizure on vocalization behavior in neonatal mice.
- To examine the impact of early life seizures on the phosphoinositide 3-kinase|serine/threonine kinase|mammalian target of rapamycin (PI3K-Akt-mTOR) and canonical Wingless-Int (Wnt) signaling pathways.
Main Methods:
- Neonatal mice (postnatal day 10) received kainic acid or vehicle injection, inducing status epilepticus.
- Isolation-induced ultrasonic vocalizations (50-kHz calls) were recorded on postnatal days 11 and 12.
- Western blotting analyzed the PI3K-Akt-mTOR pathway and phosphorylated fragile × mental retardation protein in the hippocampus on postnatal day 12.
Main Results:
- A significant, male-specific decrease in the quantity and duration of 50-kHz calls was observed post-seizure.
- Male mice exhibited sex-specific alterations in the PI3K-Akt-mTOR pathway within the hippocampus.
- Changes in phosphorylated fragile × mental retardation protein were also noted in male hippocampi.
Conclusions:
- Early life seizures disrupt communication behavior in neonatal mice.
- Sex-specific effects of seizures on vocalization and neural pathways highlight the complexity of neurodevelopmental responses to early-life insults.
Objective:
Infant crying is a series of innate vocal patterns intended to elicit the attention of adult caregivers for fulfillment of specific needs such as pain, hunger, or hypostimulation. It is one of the earliest forms of observable communication. In neonatal rodents, this behavior has recently been investigated as a potential early behavioral marker of neural deficits in neurodevelopmental disorders. However, few studies have examined the effects of seizures on vocalization behavior during the neonatal period. The purpose of this study is to investigate the effect of a single kainate-induced early life seizure on vocalization behavior in mice. This study also investigates the subsequent effect of seizures on two pathways critical for early neural development and epileptogenesis: the phosphoinositide 3-kinase|serine/threonine kinase|mammalian target of rapamycin (PI3K-Akt-mTOR) and canonical (Wingless-Int Wnt) intracellular signaling pathways.
Methods:
On postnatal day 10, male and female 129SvEvTac mice received a single intraperitoneal injection of kainic acid (2.5 mg/kg) or vehicle injection. The kainate administration resulted in 1-2 h of status epilepticus. On postnatal days 11 and 12, the quantity and duration of isolation-induced ultrasonic vocalizations were recorded. Western blotting analyses were performed using male and female pups on postnatal day 12.
Results:
There was significant, male-specific suppression in the quantity and total duration of 50-kHz calls on postnatal day 12 following seizures. The hippocampi of male mice on this postnatal day also revealed male-specific changes in the PI3K-Akt-mTOR intracellular signaling pathway, as well as changes in phosphorylated fragile × mental retardation protein.
Significance:
These findings demonstrate that early life seizures can disrupt communication behavior in neonatal mice.
