ArticleMolecular psychiatry2018
Identifying specific prefrontal neurons that contribute to autism-associated abnormalities in physiology and social behavior.
Article in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed.
- Loss of Zmiz1 in Mice Leads to Impaired Cortical Development and Autistic-Like Behaviors.Biological psychiatry · 2026Article
- Graph theory identifies altered prefrontal microcircuit organization in Shank3 mice, a mouse Model of autism.Cell reports · 2026Article
- Disrupted Development of the mPFC-Thalamic Circuit in Shank3Molecular psychiatry · 2026Article
- Medial prefrontal cortex neurons integrate amygdala and hypothalamic oxytocin signals to mediate stress-induced social alterations.Communications biology · 2026Article
- Behavioral and Prefrontal Circuit Deficits in a Newly DevelopedBiological psychiatry global open science · 2026Article
- Fmr1 knockout disrupts multiple intrinsic properties via reduced HCN channel activity in mediodorsal thalamocortical neurons.Experimental physiology · 2026Article
- Graph Theory Identifies Autistic Patterns in the Prefrontal Circuit of a Mouse Model of Autism.Research square · 2026Article
- Early postnatal dysfunction of ACC PV interneurons in Shank3BMolecular psychiatry · 2025Article
- Leveraging Fiber Photometry to Decipher Neural Circuits Underlying Anxiety in Mice.Fundamental & clinical pharmacology · 2025Review
- Prenatal valproic acid on the basis of gestational diabetes also induces autistic behavior and disrupts myelination and oligodendroglial maturation slightly in offspring.Translational psychiatry · 2025Article
- Article
- Context-invariant socioemotional encoding by prefrontal ensembles.Nature communications · 2025Article
- A cell-type-specific epigenetic mechanism encodes social investigatory behavior via Lrhcn1 and Hcn1.Science advances · 2025Article
- A molecularly defined mPFC-BLA circuit specifically regulates social novelty preference.Science advances · 2025Article
- Fine-tuning of dopamine receptor signaling with aripiprazole counteracts ketamine's dissociative action, but not its antidepressant effect.Translational psychiatry · 2025Article
- Single-nucleotide polymorphism analysis accurately predicts multiple impairments in hippocampal activity and memory performance in a murine model of idiopathic autism.Scientific reports · 2025Article
- Prenatal modulation of NADPH-oxidase reverses the deranged GABA switch and rescues behavioral deficits in valproate ASD rat model.Frontiers in pharmacology · 2025Article
- Prelimbic cortex perineuronal net expression and social behavior: Impact of adolescent intermittent ethanol exposure.Neuropharmacology · 2025Article
- Synaptotagmin-11 deficiency mediates schizophrenia-like behaviors in mice via dopamine over-transmission.Nature communications · 2024Article
- Prefrontal cortical circuits in social behaviors: an overview.Journal of Zhejiang University. Science. B · 2024Review
37 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors.
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Abstract
Functional imaging and gene expression studies both implicate the medial prefrontal cortex (mPFC), particularly deep-layer projection neurons, as a potential locus for autism pathology. Here, we explored how specific deep-layer prefrontal neurons contribute to abnormal physiology and behavior in mouse models of autism. First, we find that across three etiologically distinct models-in utero valproic acid (VPA) exposure, CNTNAP2 knockout and FMR1 knockout-layer 5 subcortically projecting (SC) neurons consistently exhibit reduced input resistance and action potential firing. To explore how altered SC neuron physiology might impact behavior, we took advantage of the fact that in deep layers of the mPFC, dopamine D2 receptors (D2Rs) are mainly expressed by SC neurons, and used D2-Cre mice to label D2R+ neurons for calcium imaging or optogenetics. We found that social exploration preferentially recruits mPFC D2R+ cells, but that this recruitment is attenuated in VPA-exposed mice. Stimulating mPFC D2R+ neurons disrupts normal social interaction. Conversely, inhibiting these cells enhances social behavior in VPA-exposed mice. Importantly, this effect was not reproduced by nonspecifically inhibiting mPFC neurons in VPA-exposed mice, or by inhibiting D2R+ neurons in wild-type mice. These findings suggest that multiple forms of autism may alter the physiology of specific deep-layer prefrontal neurons that project to subcortical targets. Furthermore, a highly overlapping population-prefrontal D2R+ neurons-plays an important role in both normal and abnormal social behavior, such that targeting these cells can elicit potentially therapeutic effects.
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