Jewett M E, Kronauer R E
Division of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138, USA.
J Theor Biol. 1998 Jun 21;192(4):455-65. doi: 10.1006/jtbi.1998.0667.
In 1990, Kronauer proposed a mathematical model of the effects of light on the human circadian pacemaker. Although this model predicted many general features of the response of the human circadian pacemaker to light exposure, additional data now available enable us to refine the original model. We first refined the original model by incorporating the results of a dose response curve to light into the model's predicted relationship between light intensity and the strength of the drive onto the pacemaker. Data from three bright light phase resetting experiments were then used to refine the amplitude recovery characteristics of the model. Finally, the model was tested and further refined using data from an extensive phase resetting experiment in which a 3-cycle bright light stimulus was presented against a background of dim light. In order to describe the results of the four resetting experiments, the following major refinements to the original model were necessary: (i) the relationship between light intensity (I) and drive onto the pacemaker was reduced from I1/3 to I0.23 for light levels between 150 and 10,000 lux; (ii) the van der Pol oscillator from the original model was replaced with a higher-order limit cycle oscillator so that amplitude recovery is slower near the singularity and faster near the limit cycle; (iii) a direct effect of light on circadian period (tau x) was incorporated into the model such that as I increases, tau x decreases, which is in accordance with "Aschoff's rule". This refined model generates the following testable predictions: it should be difficult to enhance normal circadian amplitude via bright light; near the critical point of a type 0 phase response curve (PRC) the slope should be steeper than it is in a type 1 PRC; and circadian period measured during forced desynchrony should be directly affected by ambient light intensity.
1990年，克罗瑙尔提出了一个关于光对人体昼夜节律起搏器影响的数学模型。尽管该模型预测了人体昼夜节律起搏器对光照反应的许多一般特征，但现有的更多数据使我们能够完善原始模型。我们首先通过将光剂量反应曲线的结果纳入模型预测的光强度与作用于起搏器的驱动强度之间的关系，对原始模型进行了完善。然后，利用来自三个强光相位重置实验的数据来完善模型的振幅恢复特性。最后，使用来自一个广泛的相位重置实验的数据对模型进行测试和进一步完善，在该实验中，在暗光背景下呈现了一个3周期的强光刺激。为了描述这四个重置实验的结果，对原始模型进行了以下主要完善：(i) 对于150至10000勒克斯之间的光照水平，光强度（I）与作用于起搏器的驱动之间的关系从I1/3降至I0.23；(ii) 原始模型中的范德波尔振荡器被一个高阶极限环振荡器所取代，以便在奇点附近振幅恢复较慢，在极限环附近较快；(iii) 将光对昼夜节律周期（tau x）的直接影响纳入模型，使得随着I增加，tau x减小，这与 “阿绍夫法则” 一致。这个完善后的模型产生了以下可测试的预测：通过强光增强正常昼夜节律振幅应该很困难；在0型相位反应曲线（PRC）的临界点附近，斜率应该比1型PRC中的更陡；在强制不同步期间测量的昼夜节律周期应该直接受到环境光强度的影响。
