CA2+ REGULATION IN THE PRESYNAPTIC TERMINALS OF GOLDFISH RETINAL BIPOLAR CELLS

1. To investigate regulation of the intracellular free Ca2+ concentrat ion ([Ca2+](i)) in presynaptic terminals, the Ca2+ current (I-Ca) and [Ca2+](i) in axon terminals were simultaneously monitored in acutely d issociated retinal bipolar cells under whole-cell voltage clamp. 2. Th e recovery phase of the Ca2+ transient, which was evoked by activation of I-Ca, became slower when the Na+-Ca2+ exchanger was suppressed by removing extracellular Na+. 3. Inhibition of the plasma membrane Ca2pump produced by raising extracellular pH to 8.4 increased the basal [ Ca2+](i) and caused incomplete recovery from the Ca2+ transient. These effects were not observed in orthovanadate-loaded bipolar cells. 4. T he Ca2+ transient was not significantly affected by ryanodine, caffein e, thapsigargin, Ruthenium Red or FCCP. Internal Ca2+ stores may not p articipate in shaping the Ca2+ transient. 5. The ratio of the peak amp litude of the Ca2+ transient to the total amount of Ca2+ influx became smaller as the size of the Ca2+ influx increased. This action was not affected by blockage of Ca2+ transporters in the plasma membrane, or by reduction of the rate of Ca2+ influx. The peak amplitude of the Ca2 + transient seemed to be determined by Ca2+ buffering substances with a positive co-operativity.