A common computational and neural anomaly across mouse models of autism DOI Creative Commons
Jean‐Paul Noel, Edoardo Balzani, Luigi Acerbi

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Май 8, 2024

Abstract Computational psychiatry has suggested that humans within the autism spectrum disorder (ASD) inflexibly update their expectations (i.e., Bayesian priors). Here, we leveraged high-yield rodent psychophysics (n = 75 mice), extensive behavioral modeling (including principled and heuristics), (near) brain-wide single cell extracellular recordings (over 53k units in 150 brain areas) to ask (1) whether mice with different genetic perturbations associated ASD show this same computational anomaly, if so, (2) what neurophysiological features are shared across genotypes subserving deficit. We demonstrate harboring mutations Fmr1 , Cntnap2 Shank3B a blunted of priors during decision-making. Neurally, differentiating factor between animals flexibly updating was shift weighting prior encoding from sensory frontal cortices. Further, mouse models areas showed preponderance coding for deviations animals’ long-run prior, responses did not differentiate expected unexpected observations. These findings distinct instantiations may yield common phenotypes.

Язык: Английский

A common computational and neural anomaly across mouse models of autism DOI Creative Commons
Jean‐Paul Noel, Edoardo Balzani, Luigi Acerbi

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Май 8, 2024

Abstract Computational psychiatry has suggested that humans within the autism spectrum disorder (ASD) inflexibly update their expectations (i.e., Bayesian priors). Here, we leveraged high-yield rodent psychophysics (n = 75 mice), extensive behavioral modeling (including principled and heuristics), (near) brain-wide single cell extracellular recordings (over 53k units in 150 brain areas) to ask (1) whether mice with different genetic perturbations associated ASD show this same computational anomaly, if so, (2) what neurophysiological features are shared across genotypes subserving deficit. We demonstrate harboring mutations Fmr1 , Cntnap2 Shank3B a blunted of priors during decision-making. Neurally, differentiating factor between animals flexibly updating was shift weighting prior encoding from sensory frontal cortices. Further, mouse models areas showed preponderance coding for deviations animals’ long-run prior, responses did not differentiate expected unexpected observations. These findings distinct instantiations may yield common phenotypes.

Язык: Английский

Процитировано

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