Potentiation of Ca2+ transients in the presynaptic terminals of goldfish retinal bipolar cells.
1. To study a possible contribution of intracellular Ca2+ stores to the presynaptic Ca2+ regulation, the Ca2+ current (ICa) and the intracellular free Ca2+ concentration ([Ca2+]i) were simultaneously monitored in isolated goldfish retinal bipolar cells using the whole-cell voltage clamp procedure and fura-2 fluorimetry. 2. The Ca2+ transient triggered by the activation of ICa was potentiated when [Ca2+]i was increased by applying either a prepulse or a small steady depolarization. The potentiation seemed to be partly due to the release of Ca2+ from intracellular Ca2+ stores. 3. The intracellular Ca2+ release was reversibly inhibited by caffeine but was not affected by ryanodine, suggesting that Ca2+ is released through intracellular Ca2+ channels which differ from ryanodine receptor channels. 4. These results suggest that the intracellular Ca2+ release may contribute to the facilitation of transmitter release.
Kobayashi
K
K
Department of Psychology, Faculty of Letters, University of Tokyo, Japan.
Sakaba
T
T
Tachibana
M
M
D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D006054:Goldfish; D066298:In Vitro Techniques; D007424:Intracellular Fluid / Q000187:drug effects / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects; D018408:Patch-Clamp Techniques; D017729:Presynaptic Terminals / Q000187:drug effects / Q000378:metabolism*; D012160:Retina / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism
D015220:Calcium Channels; D002110:Caffeine; D002118:Calcium