Kenyon Garrett T, Moore Bartlett, Jeffs Janelle, Denning Kate S, Stephens Greg J, Travis Bryan J, George John S, Theiler James, Marshak David W
P-21, Biophysics, Los Alamos National Laboratory, Los Alamos, NM 87545, USA.
Vis Neurosci. 2003 Sep-Oct;20(5):465-80. doi: 10.1017/s0952523803205010.
High-frequency oscillatory potentials (HFOPs) have been recorded from ganglion cells in cat, rabbit, frog, and mudpuppy retina and in electroretinograms (ERGs) from humans and other primates. However, the origin of HFOPs is unknown. Based on patterns of tracer coupling, we hypothesized that HFOPs could be generated, in part, by negative feedback from axon-bearing amacrine cells excited via electrical synapses with neighboring ganglion cells. Computer simulations were used to determine whether such axon-mediated feedback was consistent with the experimentally observed properties of HFOPs. (1) Periodic signals are typically absent from ganglion cell PSTHs, in part because the phases of retinal HFOPs vary randomly over time and are only weakly stimulus locked. In the retinal model, this phase variability resulted from the nonlinear properties of axon-mediated feedback in combination with synaptic noise. (2) HFOPs increase as a function of stimulus size up to several times the receptive-field center diameter. In the model, axon-mediated feedback pooled signals over a large retinal area, producing HFOPs that were similarly size dependent. (3) HFOPs are stimulus specific. In the model, gap junctions between neighboring neurons caused contiguous regions to become phase locked, but did not synchronize separate regions. Model-generated HFOPs were consistent with the receptive-field center dynamics and spatial organization of cat alpha cells. HFOPs did not depend qualitatively on the exact value of any model parameter or on the numerical precision of the integration method. We conclude that HFOPs could be mediated, in part, by circuitry consistent with known retinal anatomy.
在猫、兔、蛙以及泥螈的视网膜神经节细胞中，以及在人类和其他灵长类动物的视网膜电图（ERG）中，均记录到了高频振荡电位（HFOPs）。然而，HFOPs的起源尚不清楚。基于示踪剂耦合模式，我们推测HFOPs可能部分由含轴突无长突细胞通过与相邻神经节细胞的电突触兴奋产生的负反馈所引发。利用计算机模拟来确定这种轴突介导的反馈是否与HFOPs的实验观测特性相符。（1）神经节细胞的脉冲序列直方图（PSTHs）中通常不存在周期性信号，部分原因是视网膜HFOPs的相位随时间随机变化，且仅与刺激有微弱的锁定关系。在视网膜模型中，这种相位变异性是由轴突介导的反馈的非线性特性与突触噪声共同导致的。（2）HFOPs随刺激大小增加，直至达到感受野中心直径的数倍。在模型中，轴突介导的反馈在大的视网膜区域汇聚信号，产生了类似大小依赖性的HFOPs。（3）HFOPs具有刺激特异性。在模型中，相邻神经元之间的缝隙连接使相邻区域相位锁定，但未使不同区域同步。模型生成的HFOPs与猫α细胞的感受野中心动态和空间组织一致。HFOPs在性质上并不依赖于任何模型参数的精确值或积分方法的数值精度。我们得出结论，HFOPs可能部分由与已知视网膜解剖结构相符的电路介导。
