ArticleMolecular psychiatry2024
Adenosine mediates the amelioration of social novelty deficits during rhythmic light treatment of 16p11.2 deletion female mice.
Article in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Review
- High intensity 40 Hz flicker improves amyloid pathology and cognition with autophagy in 3xTg mice.iScience · 2026Article
- A locus coeruleus-centric framework for novelty, salience, and gamma oscillations: implications for neurostimulation, aging, and disease.Frontiers in aging neuroscience · 2026Article
- Light-based 40 Hz sensory therapy for brain disorders: physiological basis, therapeutic mechanisms, and future prospects.Frontiers in medicine · 2026Review
- TrkB modulates parvalbumin interneuron excitability and spatial memory enhancement induced by long-term rhythmic light flicker.iScience · 2025Article
- Parvalbumin Interneuron-Dependent Hippocampal Neurogenesis Evoked by Prolonged Rhythmic Light Flicker.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The "don't eat me" signal CD47 is associated with microglial phagocytosis defects and autism-like behaviors in 16p11.2 deletion mice.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Advancing personalized digital therapeutics: integrating music therapy, brainwave entrainment methods, and AI-driven biofeedback.Frontiers in digital health · 2025Review
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Authors and funding
12 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Non-invasive brain stimulation therapy for autism spectrum disorder (ASD) has shown beneficial effects. Recently, we and others demonstrated that visual sensory stimulation using rhythmic 40 Hz light flicker effectively improved cognitive deficits in mouse models of Alzheimer's disease and stroke. However, whether rhythmic visual 40 Hz light flicker stimulation can ameliorate behavioral deficits in ASD remains unknown. Here, we show that 16p11.2 deletion female mice exhibit a strong social novelty deficit, which was ameliorated by treatment with a long-term 40 Hz light stimulation. The elevated power of local-field potential (LFP) in the prefrontal cortex (PFC) of 16p11.2 deletion female mice was also effectively reduced by 40 Hz light treatment. Importantly, the 40 Hz light flicker reversed the excessive excitatory neurotransmission of PFC pyramidal neurons without altering the firing rate and the number of resident PFC neurons. Mechanistically, 40 Hz light flicker evoked adenosine release in the PFC to modulate excessive excitatory neurotransmission of 16p11.2 deletion female mice. Elevated adenosine functioned through its cognate A
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