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褪黑素的抑制对光极为敏感,主要由人类的黑视蛋白驱动。

Melatonin suppression is exquisitely sensitive to light and primarily driven by melanopsin in humans.

机构信息

Lyon Neuroscience Research Center, Integrative Physiology of the Brain Arousal Systems, Waking team, Inserm UMRS 1028, CNRS UMR 5292, Université Claude Bernard Lyon 1, Université de Lyon, F-69000, Lyon, France.

Department of Visual Neuroscience, Singapore Eye Research Institute, Singapore.

出版信息

J Pineal Res. 2019 May;66(4):e12562. doi: 10.1111/jpi.12562. Epub 2019 Mar 1.

Abstract

INTRODUCTION

Light elicits a range of non-visual responses in humans. Driven predominantly by intrinsically photosensitive retinal ganglion cells (ipRGCs), but also by rods and/or cones, these responses include melatonin suppression. A sigmoidal relationship has been established between melatonin suppression and light intensity; however, photoreceptoral involvement remains unclear.

METHODS AND RESULTS

In this study, we first modelled the relationships between alpha-opic illuminances and melatonin suppression using an extensive dataset by Brainard and colleagues. Our results show that (a) melatonin suppression is better predicted by melanopic illuminance compared to other alpha-opic illuminances, (b) melatonin suppression is predicted to occur at levels as low as ~1.5 melanopic lux (melanopsin-weighted irradiance 0.2 µW/cm ), (c) saturation occurs at 305 melanopic lux (melanopsin-weighted irradiance 36.6 µW/cm ). We then tested this melanopsin-weighted illuminance-response model derived from Brainard and colleagues' data and show that it predicts equally well melatonin suppression data from our laboratory, although obtained using different intensities and exposure duration.

DISCUSSION

Together, our findings suggest that melatonin suppression by monochromatic lights is predominantly driven by melanopsin and that it can be initiated at extremely low melanopic lux levels in experimental conditions. This emphasizes the concern of the non-visual impacts of low light intensities in lighting design and light-emitting devices.

摘要

简介

光在人类中引发了一系列非视觉反应。这些反应主要由内在感光视网膜神经节细胞(ipRGC)驱动,但也由视杆细胞和/或视锥细胞驱动,包括褪黑素抑制。褪黑素抑制与光强度之间已经建立了一种 S 型关系;然而,光感受器的参与仍不清楚。

方法和结果

在这项研究中,我们首先使用 Brainard 及其同事的大量数据集来模拟 alpha-opic 照度与褪黑素抑制之间的关系。我们的结果表明:(a)与其他 alpha-opic 照度相比,褪黑素抑制更能被视黑素照度预测;(b)褪黑素抑制预计在低至约 1.5 视黑素 lux(视黑素加权辐照度 0.2µW/cm)的水平发生;(c)在 305 视黑素 lux(视黑素加权辐照度 36.6µW/cm)时达到饱和。然后,我们测试了从 Brainard 及其同事的数据中得出的这种视黑素加权照度-反应模型,并表明它同样可以很好地预测我们实验室获得的褪黑素抑制数据,尽管使用了不同的强度和暴露持续时间。

讨论

总的来说,我们的发现表明,单色光的褪黑素抑制主要由视黑素驱动,并且在实验条件下可以在极低的视黑素 lux 水平下引发。这强调了在照明设计和发光设备中低光强度的非视觉影响的关注。

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