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Altered socio-affective communication and amygdala development in mice with protocadherin10-deficient interneurons
Tania Aerts1, Anneleen Boonen1, Lieve Geenen1
1Faculty of Science, Department of Biology, Division of Animal Physiology and Neurobiology, Lab of Developmental Neurobiology, KU Leuven , Leuven 3000, Belgium.
Insights
Loss of protocadherin10 (PCDH10) in specific brain interneurons alters social communication in mice, offering insights into autism spectrum disorder (ASD) development.
Area of Science:
- Neuroscience
- Genetics
- Developmental Biology
Background:
- Autism spectrum disorder (ASD) involves social and communication deficits.
- Protocadherin10 (PCDH10), a cell adhesion molecule, is implicated in ASD.
- PCDH10 plays a role in neural circuit formation during development.
Purpose of the Study:
- To investigate the role of PCDH10 in neural development and socio-affective communication.
- To determine the specific contribution of PCDH10 in interneurons to ASD-related behaviors.
Main Methods:
- Utilized a conditional knockout (cKO) mouse model to selectively delete Pcdh10 in Gsh2-lineage interneurons.
- Analyzed vocalizations and acoustic features in heterozygous Pcdh10 cKO pups.
- Examined Pcdh10 expression patterns in the developing mouse brain, including the amygdala.
Main Results:
- PCDH10 is expressed in inhibitory and excitatory neurons in the amygdala during development.
- Selective deletion of Pcdh10 in Gsh2-lineage interneurons led to altered vocalization rates and acoustic properties.
- These communication changes were linked to potential alterations in anxiety levels.
Conclusions:
- Loss of PCDH10 specifically in interneurons contributes to socio-affective communication deficits relevant to ASD.
- The findings highlight the critical role of PCDH10 in interneuron function and social behavior.
- PCDH10's function in interneurons may be a key factor in ASD pathogenesis.
Abstract:
Autism spectrum disorder (ASD) is a group of neurodevelopmental conditions associated with deficits in social interaction and communication, together with repetitive behaviours. The cell adhesion molecule protocadherin10 (PCDH10) is linked to ASD in humans. Pcdh10 is expressed in the nervous system during embryonic and early postnatal development and is important for neural circuit formation. In mice, strong expression of Pcdh10 in the ganglionic eminences and in the basolateral complex (BLC) of the amygdala was observed at mid and late embryonic stages, respectively. Both inhibitory and excitatory neurons expressed Pcdh10 in the BLC at perinatal stages and vocalization-related genes were enriched in Pcdh10-expressing neurons in adult mice. An epitope-tagged Pcdh10-HAV5 mouse line revealed endogenous interactions of PCDH10 with synaptic proteins in the young postnatal telencephalon. Nuanced socio-affective communication changes in call emission rates, acoustic features and call subtype clustering were primarily observed in heterozygous pups of a conditional knockout (cKO) with selective deletion of Pcdh10 in Gsh2-lineage interneurons. These changes were less prominent in heterozygous ubiquitous Pcdh10 KO pups, suggesting that altered anxiety levels associated with Gsh2-lineage interneuron functioning might drive the behavioural effects. Together, loss of Pcdh10 specifically in interneurons contributes to behavioural alterations in socio-affective communication with relevance to ASD.
