Evidence map›Paper›PMID 37745660›Full record

ReviewFrontiers in neurology2023

Circuit-level theories for sensory dysfunction in autism: convergence across mouse models.

Hannah R Monday, Han Chin Wang, Daniel E Feldman

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Degraded sensory coding in a mouse model ofbioRxiv : the preprint server for biology · 2025
    Article
  4. Altered Primary Somatosensory Neuron Development in a Pten Heterozygous Model for Autism Spectrum Disorder.Autism research : official journal of the International Society for Autism Research · 2025
    Article
  5. Article
  6. Article
  7. Atypical Retinal Ganglion Cell Function in a Mouse Model of Fragile X Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Hannah R MondayDepartment of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA, United States.
Han Chin WangDepartment of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA, United States.
Daniel E FeldmanDepartment of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA, United States.
University of California, Berkeley · US

Funding

Rapid inhibitory circuit plasticity as a homeostatic mechanism in cerebral cortexR01NS105333 · NINDS · UNIVERSITY OF CALIFORNIA BERKELEY · PI FELDMAN, DANIEL · 2018 to 2022
$1.7M
Physiological and Molecular Mechanisms of Impaired PV Circuit Homeostasis in Autism Mouse ModelsF32NS126310 · NINDS · UNIVERSITY OF CALIFORNIA BERKELEY · PI MONDAY, HANNAH · 2023 to 2025
$199k
NINDS NIH HHS F32 NS126310NINDS NIH HHS R01 NS105333
6 · The paper itself

Abstract

Individuals with autism spectrum disorder (ASD) exhibit a diverse range of behavioral features and genetic backgrounds, but whether different genetic forms of autism involve convergent pathophysiology of brain function is unknown. Here, we analyze evidence for convergent deficits in neural circuit function across multiple transgenic mouse models of ASD. We focus on sensory areas of neocortex, where circuit differences may underlie atypical sensory processing, a central feature of autism. Many distinct circuit-level theories for ASD have been proposed, including increased excitation-inhibition (E-I) ratio and hyperexcitability, hypofunction of parvalbumin (PV) interneuron circuits, impaired homeostatic plasticity, degraded sensory coding, and others. We review these theories and assess the degree of convergence across ASD mouse models for each. Behaviorally, our analysis reveals that innate sensory detection behavior is heightened and sensory discrimination behavior is impaired across many ASD models. Neurophysiologically, PV hypofunction and increased E-I ratio are prevalent but only rarely generate hyperexcitability and excess spiking. Instead, sensory tuning and other aspects of neural coding are commonly degraded and may explain impaired discrimination behavior. Two distinct phenotypic clusters with opposing neural circuit signatures are evident across mouse models. Such clustering could suggest physiological subtypes of autism, which may facilitate the development of tailored therapeutic approaches.

Indexed as

autismcircuitcortexexcitabilityinhibitionneural codingsensorytheory

Identifiers

PMID37745660
PMCPMC10513044
OpenAlexW4386498984

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.