Pepperberg D R
Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, College of Medicine, 60612, USA.
Vis Neurosci. 1998 Nov-Dec;15(6):1067-78. doi: 10.1017/s0952523898156079.
Recovery kinetics of the saturating photocurrent response in amphibian rods suggest regulation of the visual signal by a first-order deactivation reaction with an exponential time constant (tau(c)) of about 2 s. The original hypothesis that tau(c) represents the lifetime of activated rhodopsin (R*) in a single-step deactivation appears at odds with several recent findings, for example, that Ca2+, a known regulator of the enzymatic phosphorylation of R*, does not regulate the value of tau(c). A recently proposed alternative hypothesis, that tau(c) is the lifetime of activated transducin and that the R* lifetime is relatively short (approximately 0.4 s), appears consistent with the Ca2+ data but is difficult to reconcile with a high specific catalytic activity of R*. The present theoretical study proposes a rate-equation model of R* activation and deactivation in amphibian rods that is generally consistent with observed properties of the tau(c)-associated reaction and the action of Ca2+ as well as with the stereotyped nature of the single-photon response. The model is developed by considering the effect of background light on a time-dependent variable, Reff, defined as the effective total level of R activity. Central starting assumptions are that Ca2+ reduction mediates the effect of background light on Reff(t) and that background desensitization of the photocurrent flash response derives from this action of Ca2+. Construction of the model is guided by criteria based on previous experimental findings. Among these are the approximate constancy of background desensitization expressed at near-peak and later times in the flash response, and the large (approximately 10-fold) dynamic range of this desensitization. The proposed model hypothesizes that an event regulated by Ca2+ feedback causes activated rhodopsin to become susceptible to a two-phase, stochastic deactivation process, the second phase of which is characterized by tau(c). A central prediction of the model is the regulated transition of flash-activated R to "R**", a state exhibiting greatly increased catalytic activity.
两栖动物视杆细胞中饱和光电流响应的恢复动力学表明，视觉信号受一级失活反应调节，其指数时间常数（tau(c)）约为2秒。最初的假设认为，tau(c)代表单步失活中活化视紫红质（R*）的寿命，但这一假设与最近的一些发现不一致，例如，已知的R酶促磷酸化调节剂Ca2+并不调节tau(c)的值。最近提出的另一种假设认为，tau(c)是活化转导蛋白的寿命，而R的寿命相对较短（约0.4秒），这一假设似乎与Ca2+数据一致，但难以与R的高比催化活性相协调。目前的理论研究提出了一个两栖动物视杆细胞中R激活和失活的速率方程模型，该模型总体上与tau(c)相关反应的观察特性、Ca2+的作用以及单光子响应的刻板性质一致。该模型是通过考虑背景光对一个随时间变化的变量Reff的影响而开发的，Reff定义为R活性的有效总水平。核心起始假设是，Ca2+的减少介导了背景光对Reff(t)的影响，并且光电流闪光响应的背景脱敏源于Ca2+的这一作用。模型的构建以基于先前实验结果的标准为指导。其中包括在闪光响应的近峰值和后期表现出的背景脱敏的近似恒定性，以及这种脱敏的大（约10倍）动态范围。所提出的模型假设，由Ca2+反馈调节的一个事件会使活化视紫红质易于发生两阶段的随机失活过程，其中第二阶段的特征是tau(c)。该模型的一个核心预测是闪光激活的R向“R”的调节转变，“R*”是一种催化活性大大增加的状态。
