QUANTITATIVE ANALYSIS OF INFORMATION TRANSMISSION IN THE RETINAL RIBBON SYNAPSES

对视网膜双极细胞释放递质的机制进行了电生理学和形态学研究。我们得到了以下结果：1.对金鱼双极细胞轴突末端进行全细胞钳制，测量胞吐相关的膜电容变化。用富含谷氨酸受体的神经元作为传感器，同时对释放的谷氨酸进行电生理监测。两极末端长时间的去极化导致谷氨酸的相性释放(由于第一和第二池)，随后是一个小的紧张性释放，这表明第三池的存在。金鱼双极细胞突触前终末蛋白激酶C(PKC)的激活增加了谷氨酸的释放量。双脉冲实验表明，这种增加归因于第二个池的池大小的增加。EM研究表明，PKC激活后，突触小泡聚集在突触带附近。在Newt视网膜切片制备中，一对双极细胞和神经节细胞同时被全细胞钳制。双极细胞的去极化在神经节细胞中诱发EPSC。阻断谷氨酸转运体导致诱发的EPSC延长。谷氨酸转运体实际上参与了诱发的EPSC的形成和光诱导的反应。在制作小鼠视网膜切片的过程中，观察了双极终末GABAc受体的功能。当GABAc受体完整时，无长突细胞的光诱导电流主要由AMPA受体介导的电流组成。阻断GABAc受体后，光诱导电流由AMPA受体介导的电流组成，其次是NMDA受体介导的电流。GABAc介导的无长突细胞反馈调节双极细胞谷氨酸的释放量。

Mechanisms of transmitter release from retinal bipolar cells were investigated electrophysiologically and morphologically. We obtained the following results.1. Axon terminals of goldfish bipolar cells were whole-cell clamped, and the membrane capacitance changes associated with exocytosis were measured. The released glutamate was simultaneously monitored electrophysiologically with a glutamate receptor rich neuron as a sensor. Prolonged depolarization of bipolar terminals resulted in a phasic release of glutamate (due to the first and second pools), which was followed by a small tonic release, suggesting the presence of the third pool.2. Activation of protein kinase C (PKC) in the presynaptic terminals of goldfish bipolar cells increased the amount of glutamate release. The double-pulse experiments revealed that the increase was ascribed to the increase in the pool size of the second pool. EM studies indicated that synaptic vesicles accumulated near the synaptic ribbons after the PKC activation.3. A pair of bipolar and ganglion cells was simultaneously whole-cell clamped in the slice preparation of the newt retina. Depolarization of a bipolar cell evoked an EPSC in the ganglion cell. Blockade of glutamate transporters resulted in the prolongation of the evoked EPSC.Glutamate transporters actually contribute to the shaping of the evoked EPSC and the light-induced responses.4. The function of GABA_c-receptors at bipolar terminals was examined in the slice preparation of the mouse retina. When GABA_c-receptors were intact, the light-induced current in amacrine cells composed mainly of the AMPA-receptor mediated current. After the blockage of GABA_c receptors, the light-induced current composed of the AMPA-receptor mediated current, which was followed by the NMDA-receptor mediated current. GABA_c-mediated feedback from amacrine cells regulate the amount of glutamate release from bipolar cells.