Shank3 mutation disrupts affective touch encoding in the dorsal medial prefrontal cortex of Beagle dogs
- 1Hubei University
Abstract
Individuals with autism spectrum disorder (ASD) often show aversion to affective touch (AT). However, the neural mechanism of this abnormality in cortices remains poorly understood probably due to the lack of effective animal models. Here, we used a canine model to address this issue by leveraging the intimate dog-human interactions. In a newly-designed heterospecific AT paradigm, we found that dogs carrying mutations in Shank3, a high-risk gene for ASD, avoided human AT. In vivo single-unit recording analysis showed that AT-evoked oscillations in the dorsal medial prefrontal cortex (dmPFC) were significantly altered in Shank3 mutant dogs. Shank3 mutation also reduced the number of neurons encoding AT in the dmPFC. Importantly, the aversion to AT and altered neural processing in Shank3 mutants were largely rescued by a GABAA receptor antagonist pentylenetetrazole. Together, these findings provide neural mechanisms for abnormal AT processing in ASD and suggest potential biomarkers for therapeutic strategies.
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BibTeX
@misc{zhou2026shank3,
title = {{Shank3 mutation disrupts affective touch encoding in the dorsal medial prefrontal cortex of Beagle dogs}},
author = {Y. Zhou and Y. He and M. Dan and L. Jia and K. Guo and Y. Fang and L. Hu and X. Yu and J. Wang and D. Xing and Y. Q. Zhang},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.01.748311},
url = {https://www.biorxiv.org/content/10.64898/2026.09.01.748311v1},
note = {CC BY-NC},
}
RIS
TY - UNPB
TI - Shank3 mutation disrupts affective touch encoding in the dorsal medial prefrontal cortex of Beagle dogs
AU - Y. Zhou
AU - Y. He
AU - M. Dan
AU - L. Jia
AU - K. Guo
AU - Y. Fang
AU - L. Hu
AU - X. Yu
AU - J. Wang
AU - D. Xing
AU - Y. Q. Zhang
PY - 2026
DA - 2026/09/01
PB - bioRxiv
DO - 10.64898/2026.09.01.748311
UR - https://www.biorxiv.org/content/10.64898/2026.09.01.748311v1
AB - Individuals with autism spectrum disorder (ASD) often show aversion to affective touch (AT). However, the neural mechanism of this abnormality in cortices remains poorly understood probably due to the lack of effective animal models. Here, we used a canine model to address this issue by leveraging the intimate dog-human interactions. In a newly-designed heterospecific AT paradigm, we found that dogs carrying mutations in Shank3, a high-risk gene for ASD, avoided human AT. In vivo single-unit recording analysis showed that AT-evoked oscillations in the dorsal medial prefrontal cortex (dmPFC) were significantly altered in Shank3 mutant dogs. Shank3 mutation also reduced the number of neurons encoding AT in the dmPFC. Importantly, the aversion to AT and altered neural processing in Shank3 mutants were largely rescued by a GABAA receptor antagonist pentylenetetrazole. Together, these findings provide neural mechanisms for abnormal AT processing in ASD and suggest potential biomarkers for therapeutic strategies.
ER -