ArticleProceedings of the National Academy of Sciences of the United States of America2024
Developing forebrain synapses are uniquely vulnerable to sleep loss.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Sleep differentially modulates synaptic vesicle protein 2A and spine density across cortical regions and development.iScience · 2026Article
- Circadian Changes in CA1 LTP Are Driven by Shifts in Excitation-Inhibition Balance and Reverse Direction after Puberty in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Reverse electron transfer at mitochondrial complex I restrains dopaminergic neuron activity to promote early-life sleep inbioRxiv : the preprint server for biology · 2026Article
- The effects of sleep disturbances on patients receiving methadone treatment for opioid use disorder: cortical thickness evidence.Frontiers in psychiatry · 2026Article
- Latent mechanisms of plasticity are upregulated during sleep.Current opinion in neurobiology · 2025Review
- Choline alleviates cognitive impairment in sleep-deprived young mice via reducing neuroinflammation and altering phospholipidomic profile.Redox biology · 2025Article
- Calcineurin goes to sleep.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Re-Evaluating Recommended Optimal Sleep Duration: A Perspective on Sleep Literacy.Children (Basel, Switzerland) · 2024Review
- The E3 ubiquitin ligase TRIM9 regulates synaptic function and actin dynamics in response to netrin-1.Molecular biology of the cell · 2024Article
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Abstract
Sleep is an essential behavior that supports lifelong brain health and cognition. Neuronal synapses are a major target for restorative sleep function and a locus of dysfunction in response to sleep deprivation (SD). Synapse density is highly dynamic during development, becoming stabilized with maturation to adulthood, suggesting sleep exerts distinct synaptic functions between development and adulthood. Importantly, problems with sleep are common in neurodevelopmental disorders including autism spectrum disorder (ASD). Moreover, early life sleep disruption in animal models causes long-lasting changes in adult behavior. Divergent plasticity engaged during sleep necessarily implies that developing and adult synapses will show differential vulnerability to SD. To investigate distinct sleep functions and mechanisms of vulnerability to SD across development, we systematically examined the behavioral and molecular responses to acute SD between juvenile (P21 to P28), adolescent (P42 to P49), and adult (P70 to P100) mice of both sexes. Compared to adults, juveniles lack robust adaptations to SD, precipitating cognitive deficits in the novel object recognition task. Subcellular fractionation, combined with proteome and phosphoproteome analysis revealed the developing synapse is profoundly vulnerable to SD, whereas adults exhibit comparative resilience. SD in juveniles, and not older mice, aberrantly drives induction of synapse potentiation, synaptogenesis, and expression of perineuronal nets. Our analysis further reveals the developing synapse as a putative node of convergence between vulnerability to SD and ASD genetic risk. Together, our systematic analysis supports a distinct developmental function of sleep and reveals how sleep disruption impacts key aspects of brain development, providing insights for ASD susceptibility.
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