Cntnap2 deletion in mice causes developmentally transient alterations in auditory processing and persistent startle hyperreactivity

A recent study shows that deleting the Cntnap2 gene in mice results in temporary changes in auditory processing and a lasting heightened reaction to sudden loud noises. Autism spectrum disorder (ASD) often includes such auditory symptoms, which are believed to be partly caused by the slower development of the auditory brainstem.

Previous research has found that mutations in the Cntnap2 gene, linked to auditory processing and language development, are responsible for ASD in humans. Knocking out the Cntnap2 gene in rats has been shown to cause impairments in the auditory brainstem. However, it was unclear if mice would exhibit similar disruptions. To find out, researchers studied the development of auditory processing, reactivity, and sensory filtering in juvenile and adult Cntnap2 knockout (KO) mice.

They discovered that juvenile KO mice had larger ABR wave III amplitudes and smaller wave IV widths, which returned to normal levels in adult mice, indicating the potential for a brief hyperexcitability in the developing auditory brainstem. Furthermore, the researchers found that male KO mice exhibited a more pronounced startle response that continued into adulthood, while prepulse inhibition (PPI) remained mostly unaffected in KO mice at both ages.

These findings suggest that losing Cntnap2 in mice creates auditory brainstem problems similar to those in rats, but with species and gender-specific impacts on auditory reactivity. This indicates that the mouse model can be a useful alternative to study the neural processes behind auditory issues in ASD.