QUANTITATIVE ANALYSIS OF INFORMATION TRANSMISSION IN THE RETINAL RIBBON SYNAPSES

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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.