ArticleMolecular autism2025
Somatostatin-expressing interneurons of prefrontal cortex modulate social deficits in the Magel2 mouse model of autism.
Article in Molecular autism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Targeted Restoration of the Microbial Tryptophan Oxidative Pathway Ameliorates Autism-Like Behavioral and Synaptic Deficits.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Developmental trajectories of somatostatin-positive interneurons in the human auditory cortex from migration to maturation.Communications biology · 2026Article
- Psychedelic Modulation of Excitation/Inhibition Balance: A Dual-Phase Neurodevelopmental Model.ACS chemical neuroscience · 2026Review
- Ertugliflozin improves animal behaviours associated with oxidative stress and inflammation in a BTBRBrain communications · 2026Article
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Authors and funding
13 authors.
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Abstract
Dysfunction in social interactions is a core symptom of autism spectrum disorder (ASD). Nevertheless, the neural mechanisms underlying social deficits in ASD are poorly understood. By integrating electrophysiological, in vivo fiber photometry, viral-mediated tracing, optogenetic and pharmacological stimulation, we show reduced intrinsic excitability and hypoactivity of SOM interneurons in medial prefrontal cortex (mPFC) in Magel2-deficient mice, an established ASD model, were required to social defects. Chemogenetic inhibition of mPFC SOM-containing interneurons resulted in reduced social interaction in wild-type Magel2 mice. These sociability deficits can be rescued by optogenetic activation by excitability of SOM in the mPFC and mPFC
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