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Suppression of Cofilin function in the somatosensory cortex alters social contact behavior in the BTBR mouse inbred line

  • Iris W Riemersma
  • , Kevin G O Ike
  • , Thomas Sollie
  • , Elroy L Meijer
  • , Robbert Havekes
  • , Martien J H Kas

Research output: Contribution to JournalArticleAcademicpeer-review

Abstract

Sensory differences are a core feature of autism spectrum disorders (ASD) and are predictive of other ASD core symptoms such as social difficulties. However, the neurobiological substrate underlying the functional relationship between sensory and social functioning is poorly understood. Here, we examined whether misregulation of structural plasticity in the somatosensory cortex modulates aberrant social functioning in BTBR mice, a mouse model for autism spectrum disorder-like phenotypes. By locally expressing a dominant-negative form of Cofilin (CofilinS3D; a key regulator of synaptic structure) in the somatosensory cortex, we tested whether somatosensory suppression of Cofilin activity alters social functioning in BTBR mice. Somatosensory Cofilin suppression altered social contact and nest-hide behavior of BTBR mice in a social colony, assessed for seven consecutive days. Subsequent behavioral testing revealed that altered social functioning is related to altered tactile sensory perception; CofilinS3D-treated BTBR mice showed a time-dependent difference in the sensory bedding preference task. These findings show that Cofilin suppression in the somatosensory cortex alters social functioning in BTBR mice and that this is associated with tactile sensory processing, a critical indicator of somatosensory functioning.

Original languageEnglish
Article numberbhae136
JournalCerebral cortex (New York, N.Y. : 1991)
Volume34
Issue number4
DOIs
Publication statusPublished - 1 Apr 2024
Externally publishedYes

Bibliographical note

© The Author(s) 2024. Published by Oxford University Press.

Funding

This work was supported by the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 777394. This joint undertaking receives support from the European Union’s Horizon 2020 research and innovation program and EFPIA, SFARI, Autistica, and AUTISM SPEAKS. In addition, this work was supported by the European Union’s Horizon 2020 research and innovation program CANDY under grant agreement No 847818. Any views expressed are those of the authors and not necessarily those of the funders.

FundersFunder number
European Federation of Pharmaceutical Industries and Associations
European Union’s Horizon 2020 research and innovation program CANDY
Simons Foundation Autism Research Initiative
AUTISM
Horizon 2020 Framework Programme847818
Innovative Medicines Initiative777394

    Keywords

    • Animals
    • Mice
    • Somatosensory Cortex
    • Autism Spectrum Disorder
    • Disease Models, Animal
    • Actin Depolymerizing Factors
    • Touch

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