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Autism spectrum disorder-like behavior caused by reduced excitatory synaptic transmission in pyramidal neurons of mouse prefrontal cortex

Author

Listed:
  • Hiroaki Sacai

    (The University of Tokyo)

  • Kazuto Sakoori

    (The University of Tokyo
    The University of Tokyo Institutes for Advanced Study (UTIAS), The University of Tokyo)

  • Kohtarou Konno

    (Hokkaido University Graduate School of Medicine)

  • Kenichiro Nagahama

    (The University of Tokyo
    The University of Tokyo Institutes for Advanced Study (UTIAS), The University of Tokyo)

  • Honoka Suzuki

    (The University of Tokyo
    The University of Tokyo Institutes for Advanced Study (UTIAS), The University of Tokyo)

  • Takaki Watanabe

    (The University of Tokyo
    The University of Tokyo Institutes for Advanced Study (UTIAS), The University of Tokyo)

  • Masahiko Watanabe

    (Hokkaido University Graduate School of Medicine)

  • Naofumi Uesaka

    (The University of Tokyo
    The University of Tokyo Institutes for Advanced Study (UTIAS), The University of Tokyo
    Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University)

  • Masanobu Kano

    (The University of Tokyo
    The University of Tokyo Institutes for Advanced Study (UTIAS), The University of Tokyo)

Abstract

Autism spectrum disorder (ASD) is thought to result from deviation from normal development of neural circuits and synaptic function. Many genes with mutation in ASD patients have been identified. Here we report that two molecules associated with ASD susceptibility, contactin associated protein-like 2 (CNTNAP2) and Abelson helper integration site-1 (AHI1), are required for synaptic function and ASD-related behavior in mice. Knockdown of CNTNAP2 or AHI1 in layer 2/3 pyramidal neurons of the developing mouse prefrontal cortex (PFC) reduced excitatory synaptic transmission, impaired social interaction and induced mild vocalization abnormality. Although the causes of reduced excitatory transmission were different, pharmacological enhancement of AMPA receptor function effectively restored impaired social behavior in both CNTNAP2- and AHI1-knockdown mice. We conclude that reduced excitatory synaptic transmission in layer 2/3 pyramidal neurons of the PFC leads to impaired social interaction and mild vocalization abnormality in mice.

Suggested Citation

  • Hiroaki Sacai & Kazuto Sakoori & Kohtarou Konno & Kenichiro Nagahama & Honoka Suzuki & Takaki Watanabe & Masahiko Watanabe & Naofumi Uesaka & Masanobu Kano, 2020. "Autism spectrum disorder-like behavior caused by reduced excitatory synaptic transmission in pyramidal neurons of mouse prefrontal cortex," Nature Communications, Nature, vol. 11(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-18861-3
    DOI: 10.1038/s41467-020-18861-3
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    Cited by:

    1. Jung Ho Hyun & Kenichiro Nagahama & Ho Namkung & Neymi Mignocchi & Seung-Eon Roh & Patrick Hannan & Sarah Krüssel & Chuljung Kwak & Abigail McElroy & Bian Liu & Mingguang Cui & Seunghwan Lee & Dongmin, 2022. "Tagging active neurons by soma-targeted Cal-Light," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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