Sampath Alapakkam P, Rieke Fred
Department of Physiology and Biophysics, University of Washington, Seattle, WA 98195, USA.
Neuron. 2004 Feb 5;41(3):431-43. doi: 10.1016/s0896-6273(04)00005-4.
A threshold-like nonlinearity in signal transfer from mouse rod photoreceptors to rod bipolar cells dramatically improves the absolute sensitivity of the rod signals. The work described here reaches three conclusions about the mechanisms generating this nonlinearity. (1) The nonlinearity is caused primarily by saturation of the feedforward rod-to-rod bipolar synapse and not by feedback from horizontal or amacrine cells. This saturation renders the rod bipolar current insensitive to small changes in transmitter release from the rod. (2) Saturation occurs within the G protein cascade that couples receptors to channels in the rod bipolar dendrites, with little or no contribution from presynaptic mechanisms or saturation of the postsynaptic receptors. (3) Between 0.5 and 2 bipolar transduction channels are open in darkness at each synapse, compared to the approximately 30 channels open at the peak of the single photon response.
从小鼠视杆光感受器到视杆双极细胞的信号传递中，一种类似阈值的非线性显著提高了视杆信号的绝对灵敏度。本文所述的研究就产生这种非线性的机制得出了三个结论。（1）这种非线性主要是由前馈视杆 - 视杆双极突触的饱和引起的，而非来自水平细胞或无长突细胞的反馈。这种饱和使视杆双极电流对视杆释放递质的微小变化不敏感。（2）饱和发生在将受体与视杆双极树突中的通道偶联的G蛋白级联反应中，突触前机制或突触后受体饱和的贡献很小或没有。（3）在黑暗中，每个突触处有0.5至2个双极转导通道开放，而在单光子反应峰值时约有30个通道开放。
