ArticleNature neuroscience2025
A common computational and neural anomaly across mouse models of autism.
Article in Nature neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Computational mechanisms of perception in autism revealed using games inspired by rodent operant tasks.Science advances · 2026Article
- Social Novelty Recruits a Dysfunctional Nucleus Accumbens Ensemble That Drives Social Avoidance in abioRxiv : the preprint server for biology · 2026Article
- Multifiber Array-Based Photometry System for Multiregional Functional Mapping in the Mouse Brain.The European journal of neuroscience · 2026Article
- Intact Susceptibility to Visual Illusions in Autistic Individuals.Autism research : official journal of the International Society for Autism Research · 2025Article
- Excitatory/Inhibitory balance in autism spectrum disorders: Integrating genetic, neurotransmitter and computational perspectives.AIMS neuroscience · 2025Review
- An entropic explanation of insistence on sameness in autism.Frontiers in computational neuroscience · 2025Article
- Autism spectrum disorder variation as a computational trade-off via dynamic range of neuronal population responses.Nature neuroscience · 2024Article
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7 authors.
Funding
Abstract
Computational psychiatry studies suggest that individuals with autism spectrum disorder (ASD) inflexibly update their expectations. Here we leveraged high-yield rodent psychophysics, extensive behavioral modeling and brain-wide single-cell extracellular recordings to assess whether mice with different genetic perturbations associated with ASD show this same computational anomaly, and if so, what neurophysiological features are shared across genotypes. Mice harboring mutations in Fmr1, Cntnap2 or Shank3B show a blunted update of priors during decision-making. Compared with mice that flexibly updated their priors, inflexible updating of priors was associated with a shift in the weighting of prior encoding from sensory to frontal cortices. Furthermore, frontal areas in mouse models of ASD showed more units encoding deviations from the animals' long-run prior, and sensory responses did not differentiate between expected and unexpected observations. These findings suggest that distinct genetic instantiations of ASD may yield common neurophysiological and behavioral phenotypes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.