ArticleeLife2022
Suppressed prefrontal neuronal firing variability and impaired social representation in IRSp53-mutant mice.
Article in eLife, 2022. 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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7 citing papers in PubMed, 26 citations in OpenAlex.
- Hypoactivity, abnormal development of dendrites relevant to impaired synaptic transmission of calretinin-expressing interneurons in the medial prefrontal cortex underlies social deficits of mouse model in autism.Translational psychiatry · 2026Article
- State-dependent neuronal and network dynamics in the lateral hypothalamus across sevoflurane anesthesia-emergence revealed by microelectrode arrays.Microsystems & nanoengineering · 2026Article
- Human claustrum neurons encode uncertainty and prediction errors during aversive learning.bioRxiv : the preprint server for biology · 2026Article
- Astrocytic PERK Deficiency Drives Prefrontal Circuit Dysfunction and Depressive-Like Behaviors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell RNA sequencing reveals the immune features and viral tropism in the central nervous system of mice infected with Japanese encephalitis virus.Journal of neuroinflammation · 2024Article
- The PFC-LH-VTA pathway contributes to social deficits in IRSp53-mutant mice.Molecular psychiatry · 2023Article
- Molecular Mechanisms Underlying NMDARs Dysfunction and Their Role in ADHD Pathogenesis.International journal of molecular sciences · 2023Review
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Authors and funding
12 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Social deficit is a major feature of neuropsychiatric disorders, including autism spectrum disorders, schizophrenia, and attention-deficit/hyperactivity disorder, but its neural mechanisms remain unclear. Here, we examined neuronal discharge characteristics in the medial prefrontal cortex (mPFC) of IRSp53/Baiap2-mutant mice, which show social deficits, during social approach. We found a decrease in the proportion of IRSp53-mutant excitatory mPFC neurons encoding social information, but not that encoding non-social information. In addition, the firing activity of IRSp53-mutant neurons was less differential between social and non-social targets. IRSp53-mutant excitatory mPFC neurons displayed an increase in baseline neuronal firing, but decreases in the variability and dynamic range of firing as well as burst firing during social and non-social target approaches compared to wild-type controls. Treatment of memantine, an NMDA receptor antagonist that rescues social deficit in IRSp53-mutant mice, alleviates the reduced burst firing of IRSp53-mutant pyramidal mPFC neurons. These results suggest that suppressed neuronal activity dynamics and burst firing may underlie impaired cortical encoding of social information and social behaviors in IRSp53-mutant mice.
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