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韦伯定律的分子基础。

A molecular basis for Weber's law.

作者信息

Dawis S M

机构信息

Laboratory of Biophysics, Rockefeller University, New York, NY 10021-6399.

出版信息

Vis Neurosci. 1991 Oct;7(4):285-320. doi: 10.1017/s0952523800004806.

DOI:10.1017/s0952523800004806
PMID:1751417
Abstract

A mathematical model is presented that obeys a strong form of Weber's law--over a range of adapting and stimulus intensities, equal contrast stimuli evoke identical responses. To account for the strong Weber's law, the adaptive stage in the proposed model employs a "delayed" reverse reaction along with a power-law input. It is suggested that this Weber's law mechanism is responsible for a slow, voltage-uncorrelated component of adaptation in the vertebrate photoreceptor. A plausible biochemical mechanism is the G-protein cycle with phosphorylation of photoactivated photopigment (and binding of arrestin to the phosphorylated photopigment) as the adaptive process. In an Appendix, features of the general model and implications of a specific biochemical model are examined by computer simulation.

摘要

提出了一个数学模型,该模型遵循强形式的韦伯定律——在一系列适应强度和刺激强度范围内,相等对比度的刺激会引发相同的反应。为了解释强韦伯定律,所提出模型中的适应阶段采用了“延迟”反向反应以及幂律输入。有人认为,这种韦伯定律机制是脊椎动物光感受器中缓慢的、与电压不相关的适应成分的原因。一种合理的生化机制是以光激活的光色素磷酸化(以及抑制蛋白与磷酸化光色素的结合)作为适应过程的G蛋白循环。在附录中,通过计算机模拟研究了一般模型的特征和特定生化模型的含义。

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