Journal article

models of autism

Gogolla N, Leblanc J, Quast K, Südhof T, Fagiolini M, Hensch T ...see all

Journal of neurodevelopmental disorders, vol. 1, issue 2 (2010) pp. 172-181

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Abstract

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.

Author-supplied keywords

  • a severe neurobehavioral syndrome
  • among most
  • asd
  • autism spectrum
  • disorders
  • early
  • gaba
  • heritable neurodevelopmental disorders
  • neuroligin
  • parvalbumin
  • vpa
  • with a heterogeneous phenotype

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Authors

  • Nadine Gogolla

  • Jocelyn J Leblanc

  • Kathleen B Quast

  • Thomas Südhof

  • Michela Fagiolini

  • Takao K Hensch

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