Spectral Sensitivity of Circadian, Neuroendocrine and Neurobehavioral Effects of Light

S. Lockley
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引用次数: 6

Abstract

The mammalian eye detects light for a range of behavioral and physiological responses separate and apart from sight. In humans, ocular light exposure resets the endogenous circadian pacemaker, suppresses synthesis of the pineal hormone melatonin, enhances morning cortisol production, increases heart rate and core body temperature, induces pupillary constriction, and improves subjective and objective measures of alertness. Several lines of evidence suggest that these responses are mediated primarily via a novel photoreception system with short-wavelength sensitivity (λmax 460–480 nm) different from that used for sight. In order to compare the relative contribution of the novel photoreceptor system with the three-cone visual photopic system for multiple non-visual effects of light, we compared the responses following exposure to an equal photon density (2.8×1013 photons/cm2/s) either 460 nm (n=8) or 555 nm (n=8) monochromatic light (10 nm half-peak bandwidth) at night on circadian phase resetting, melatonin suppression and subjective and objective correlates of alertness. As compared to 555 nm exposure, 460 nm light caused twice the phase shift in the circadian melatonin rhythm, double the amount of melatonin suppression, and significantly reduced auditory reaction time and lapses of attention. Exposure to 460 nm light also preferentially suppressed delta-theta (0.5–5.5 Hz) activity and elevated high alpha power (9.5–10.5 Hz) in the waking electroencephalogram (EEG) recordings, indicating a more alert state. The short-wavelength sensitivity to the non-visual effects of light indicates that the photopic visual system is not the primary photoreceptor system mediating these responses to light, and is consistent with predominant input from the novel melanopsin-containing photosensitive retinal ganglion cells. These data also suggest that short-wavelength light may be an effective therapy for resetting the circadian system in Circadian Rhythm Sleep Disorders and could be used as a direct fatigue countermeasure in a range of clinical and occupational settings. Translation of these basic findings into real-world applications is beginning to occur but the challenge to architects and lighting designers is to provide lighting that optimizes both the visual and non-visual effects of light simultaneously and safely.
光对昼夜节律、神经内分泌和神经行为影响的光谱敏感性
哺乳动物的眼睛探测光线是为了一系列行为和生理反应,这些反应与视觉是分开的。在人类中,眼光照射可重置内源性昼夜节律起搏器,抑制松果体褪黑激素的合成,增强早晨皮质醇的产生,增加心率和核心体温,诱导瞳孔收缩,并改善主观和客观的警觉性指标。一些证据表明,这些反应主要是通过一种新型的光接收系统介导的,该系统具有短波长的灵敏度(λ最大460-480 nm),不同于用于视觉的光接收系统。为了比较新型光感受器系统与三锥视觉光感受器系统对多种非视觉光效应的相对贡献,我们比较了在夜间暴露于460 nm (n=8)或555nm (n=8)单色光(10 nm半峰带宽)下的响应,包括昼夜节律相位重置、褪黑激素抑制和主客观相关的警觉。与555nm光照相比,460 nm光照导致褪黑激素昼夜节律的相移增加一倍,褪黑激素抑制量增加一倍,听觉反应时间和注意力缺失显著减少。在清醒脑电图(EEG)记录中,暴露于460 nm光也优先抑制了δ - θ (0.5-5.5 Hz)活动,并提高了高α功率(9.5-10.5 Hz),表明更警觉的状态。对光的非视觉效应的短波敏感表明,光视系统不是介导这些对光反应的主要光感受器系统,并且与新型含黑视素的光敏视网膜神经节细胞的主要输入一致。这些数据还表明,短波长光可能是一种有效的治疗方法,可用于重置昼夜节律睡眠障碍的昼夜节律系统,并可在一系列临床和职业环境中作为直接的疲劳对策。将这些基本发现转化为现实世界的应用已经开始出现,但建筑师和照明设计师面临的挑战是提供同时安全优化光的视觉和非视觉效果的照明。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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