Smith R G, Vardi N
Department of Neuroscience, University of Pennsylvania, Philadelphia 19104-6058, USA.
Vis Neurosci. 1995 Sep-Oct;12(5):851-60. doi: 10.1017/s095252380000941x.
The AII amacrine cell of mammalian retina collects signals from several hundred rods and is hypothesized to transmit quantal "single-photon" signals at scotopic (starlight) intensities. One problem for this theory is that the quantal signal from one rod when summed with noise from neighboring rods would be lost if some mechanism did not exist for removing the noise. Several features of the AII might together accomplish such a noise removal operation: The AII is interconnected into a syncytial network by gap junctions, suggesting a noise-averaging function, and a quantal signal from one rod appears in five AII cells due to anatomical divergence. Furthermore, the AII contains voltage-gated Na+ and K+ channels and fires slow action potentials in vitro, suggesting that it could selectively amplify quantal photon signals embedded in uncorrelated noise. To test this hypothesis, we simulated a square array of AII somas (Rm = 25,000 Ohm-cm2) interconnected by gap junctions using a compartmental model. Simulated noisy inputs to the AII produced noise (3.5 mV) uncorrelated between adjacent cells, and a gap junction conductance of 200 pS reduced the noise by a factor of 2.5, consistent with theory. Voltage-gated Na+ and K+ channels (Na+: 4 nS, K+: 0.4 nS) produced slow action potentials similar to those found in vitro in the presence of noise. For a narrow range of Na+ and coupling conductance, quantal photon events (approximately 5-10 mV) were amplified nonlinearly by subthreshold regenerative events in the presence of noise. A lower coupling conductance produced spurious action potentials, and a greater conductance reduced amplification. Since the presence of noise in the weakly coupled circuit readily initiates action potentials that tend to spread throughout the AII network, we speculate that this tendency might be controlled in a negative feedback loop by up-modulating coupling or other synaptic conductances in response to spiking activity.
哺乳动物视网膜的AII无长突细胞收集来自数百个视杆细胞的信号，并且据推测在暗视（星光）强度下传递量子化的“单光子”信号。该理论面临的一个问题是，如果不存在消除噪声的机制，那么来自一个视杆细胞的量子信号与相邻视杆细胞的噪声相加时将会丢失。AII的几个特征可能共同完成这样的噪声消除操作：AII通过缝隙连接相互连接成一个合胞体网络，这表明它具有噪声平均功能，并且由于解剖学上的发散，来自一个视杆细胞的量子信号会出现在五个AII细胞中。此外，AII含有电压门控的Na⁺和K⁺通道，并且在体外能产生缓慢的动作电位，这表明它可以选择性地放大嵌入不相关噪声中的量子化光子信号。为了验证这一假设，我们使用一个房室模型模拟了由缝隙连接相互连接的AII胞体的方形阵列（膜电阻Rm = 25,000欧姆·平方厘米）。模拟的AII的噪声输入在相邻细胞之间产生了不相关的噪声（3.5毫伏），并且200皮西门子的缝隙连接电导使噪声降低了2.5倍，这与理论一致。电压门控的Na⁺和K⁺通道（Na⁺：4纳西门子，K⁺：0.4纳西门子）在有噪声的情况下产生了类似于在体外发现的缓慢动作电位。对于较窄范围的Na⁺和耦合电导，在有噪声的情况下，量子化光子事件（约为5 - 10毫伏）通过阈下再生事件被非线性放大。较低的耦合电导会产生虚假动作电位，而较大的电导会降低放大倍数。由于弱耦合电路中噪声的存在很容易引发倾向于在整个AII网络中传播的动作电位，我们推测这种倾向可能通过负反馈回路来控制，即响应于动作电位发放活动上调耦合或其他突触电导。
