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models of autism

by Nadine Gogolla, Jocelyn J Leblanc, Kathleen B Quast, Thomas Südhof, Michela Fagiolini, Takao K Hensch
Journal of neurodevelopmental disorders ()


PURPOSE: One unifying explanation for the complexity of Autism Spectrum Disorders (ASD) may lie in the disruption of excitatory/inhibitory (E/I) circuit balance during critical periods of development. We examined whether Parvalbumin (PV)-positive inhibitory neurons, which normally drive experience-dependent circuit refinement 1, are disrupted across heterogeneous ASD mouse models. METHODS: We performed a meta-analysis of PV expression in previously published ASD mouse models and analyzed two additional models, reflecting an embryonic chemical insult (prenatal valproate, VPA) or single-gene mutation identified in human patients (Neuroligin-3, NL-3 R451C). RESULTS: PV-cells were reduced in the neocortex across multiple ASD mouse models. In striking contrast to controls, both VPA and NL-3 mouse models exhibited an asymmetric PV-cell reduction across hemispheres in parietal and occipital cortices (but not the underlying area CA1). CONCLUSIONS: ASD mouse models may share a PV-circuit disruption, providing new insight into circuit development, potential prevention and treatment of autism.

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