ArticleSensors (Basel, Switzerland)2025
The Application of an Ultra-Thin, High-Density μECoG Array in Dissecting Caffeine-Induced Cortical Dynamics in Mice.
Article in Sensors (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- A Flexible Carbon Nanofiber-Modified Multi-Channel Electrode Enables High-Sensitivity Electrochemical Detection of Multiple Neuroactive Molecules.Sensors (Basel, Switzerland) · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
High-density micro-electrocorticography (μECoG) arrays offer precise spatial resolution with minimal invasiveness. This study employed a custom ultra-thin 64-channel μECoG array to investigate cortical activity in mice under chronic caffeine exposure. While caffeine is known to enhance short-term alertness, its long-term impact on sleep microarchitecture and brain connectivity is unclear. Continuous recordings from adult mice during baseline and recovery revealed that prolonged caffeine intake significantly reduced broadband power spectral density (PSD) and spindle power but increased interregional coherence and altered spindle duration and density. In contrast, six hours of sleep deprivation elevated PSD and coherence, mainly affecting sensorimotor and retrosplenial cortices. These findings validate the μECoG array's functionality and demonstrate that post-chronic caffeine withdrawal lowers cortical oscillatory power yet enhances network connectivity, whereas acute sleep loss boosts global synchrony. This work clarifies how sustained caffeine use and sleep deprivation distinctly disrupt sleep homeostasis through different neural mechanisms.
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Registered trials
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