The study delves into the role of Protocadherin10 (Pcdh10) in neurodevelopment, focusing on its expression in the amygdala and ganglionic eminences. The research highlights how Pcdh10 deficiency affects interneuron populations, leading to altered socio-affective communication patterns. By utilizing mouse models with Pcdh10 knockout, the study reveals nuanced changes in vocalization behavior, emphasizing the importance of interneurons in driving behavioral effects related to ASD.
Key findings include strong Pcdh10 expression in the basolateral complex of the amygdala during embryonic stages and its association with genes linked to vocalization behavior. The study demonstrates a reduction in interneurons within the basolateral complex due to conditional knockout of Pcdh10, resulting in altered developmental trajectories of socio-affective communication. Heterozygous pups exhibit increased isolation-induced ultrasonic vocalizations with distinct acoustic call features compared to wild-type mice.
Furthermore, the research uncovers specific clusters of call subtypes with unique developmental trajectories, suggesting a dynamic vocalization repertoire during early life. The study emphasizes that loss of Pcdh10 specifically in interneurons contributes significantly to behavioral alterations relevant to Autism Spectrum Disorder.
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by Aert... at www.biorxiv.org 01-04-2024
https://www.biorxiv.org/content/10.1101/2024.01.04.574190v1Deeper Inquiries