ArticleNature communications2025
Discrete photoentrainment of mammalian central clock is regulated by bi-stable dynamic network in the suprachiasmatic nucleus.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Defining Clock Neurons Within Distributed Circadian Circuits Through Multiscale Technologies.Journal of biological rhythms · 2026Review
- Advanced imaging strategies in cardiac organoids: bridging the gap between structural complexity and functional analysis.Cardiovascular diabetology · 2026Review
- A stress-sensing circuit signals to the central pacemaker to reprogram circadian rhythms.Science advances · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The biological clock synchronizes with the environmental light-dark cycle through circadian photoentrainment. While intracellular pathways regulating clock gene expression after light exposure in the suprachiasmatic nucleus are well studied in mammals, the neuronal circuits driving phase shifts remain unclear. Here, using a mouse model, we show that chemogenetic activation of early-night light-responsive neurons induces phase delays at any circadian time, potentially breaking the photoentrainment dead zone. In contrast, activating late-night light-responsive neurons mimics light-induced phase shifts. Using in vivo two-photon microscopy, we found that most neurons in the suprachiasmatic nucleus exhibit stochastic light responses, while a small subset is consistently activated in the early subjective night and another is inhibited in the late subjective night. Our findings suggest a dynamic bi-stable network model for circadian photoentrainment, where phase shifts arise from a functional circuit integrating signals to groups of outcome neurons, rather than a labeled-line principle seen in sensory systems.
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Registered trials
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