Evans Jennifer A, Elliott Jeffrey A, Gorman Michael R
Department of Psychology, University of California, San Diego, La Jolla, CA 92093, usa.
J Biol Rhythms. 2007 Aug;22(4):356-67. doi: 10.1177/0748730407301988.
In mammals, light entrains endogenous circadian pacemakers by inducing daily phase shifts via a photoreceptor mechanism recently discovered in retinal ganglion cells. Light that is comparable in intensity to moonlight is generally ineffective at inducing phase shifts or suppressing melatonin secretion, which has prompted the view that circadian photic sensitivity has been titrated so that the central pacemaker is unaffected by natural nighttime illumination. However, the authors have shown in several different entrainment paradigms that completely dark nights are not functionally equivalent to dimly lit nights, even when nighttime illumination is below putative thresholds for the circadian visual system. The present studies extend these findings. Dim illumination is shown here to be neither a strong zeitgeber, consistent with published fluence response curves, nor a potentiator of other zeitgebers. Nevertheless, dim light markedly alters the behavior of the free-running circadian pacemaker. Syrian hamsters were released from entrained conditions into constant darkness or dim narrowband green illumination (~0.01 lx, 1.3 x 10(-9) W/cm(2), peak lambda = 560 nm). Relative to complete darkness, constant dim light lengthened the period by ~0.3 h and altered the waveform of circadian rhythmicity. Among animals transferred from long day lengths (14 L:10 D) into constant conditions, dim illumination increased the duration of the active phase (alpha) by ~3 h relative to complete darkness. Short day entrainment (8 L:16 D) produced initially long alpha that increased further under constant dim light but decreased under complete darkness. In contrast, dim light pulses 2 h or longer produced effects on circadian phase and melatonin secretion that were small in magnitude. Furthermore, the amplitude of phase resetting to bright light and nonphotic stimuli was similar against dimly lit and dark backgrounds, indicating that the former does not directly amplify circadian inputs. Dim illumination markedly alters circadian waveform through effects on alpha, suggesting that dim light influences the coupling between oscillators theorized to program the beginning and end of subjective night. Physiological mechanisms responsible for conveying dim light stimuli to the pacemaker and implications for chronotherapeutics warrant further study.
在哺乳动物中,光通过一种最近在视网膜神经节细胞中发现的光感受器机制诱导每日相位偏移,从而使内源性昼夜节律起搏器同步。强度与月光相当的光通常在诱导相位偏移或抑制褪黑素分泌方面无效,这促使人们认为昼夜节律光敏感性已经经过调整,以使中央起搏器不受自然夜间光照的影响。然而,作者在几种不同的同步范式中表明,即使夜间光照低于昼夜节律视觉系统的假定阈值,完全黑暗的夜晚在功能上也不等同于昏暗照明的夜晚。本研究扩展了这些发现。此处表明,昏暗照明既不是一个强大的授时因子(与已发表的光通量响应曲线一致),也不是其他授时因子的增强剂。尽管如此,昏暗光线会显著改变自由运行的昼夜节律起搏器的行为。叙利亚仓鼠从同步条件下被释放到持续黑暗或昏暗的窄带绿色照明(~0.01勒克斯,1.3×10⁻⁹瓦/平方厘米,峰值波长 = 560纳米)中。相对于完全黑暗,持续的昏暗光线使周期延长了约0.3小时,并改变了昼夜节律的波形。在从长日照(14小时光照:10小时黑暗)转移到恒定条件的动物中,相对于完全黑暗,昏暗照明使活动期(α)的持续时间增加了约3小时。短日照同步(8小时光照:16小时黑暗)最初产生较长的α期,在持续昏暗光线下进一步增加,但在完全黑暗下减少。相比之下,2小时或更长时间的昏暗光脉冲对昼夜节律相位和褪黑素分泌的影响幅度较小。此外,在昏暗背景和黑暗背景下,对强光和非光刺激的相位重置幅度相似,这表明前者不会直接放大昼夜节律输入。昏暗照明通过对α期的影响显著改变昼夜节律波形,这表明昏暗光线会影响理论上用于设定主观夜晚开始和结束的振荡器之间的耦合。负责将昏暗光刺激传递到起搏器的生理机制以及对时间治疗学的影响值得进一步研究。