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Electrical resonance and Ca 2+ influx in the synaptic terminal of depolarizing bipolar cells from the Goldfish retina
Author(s) -
Burrone Juan,
Lagnado Leon
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1997.571ba.x
Subject(s) - depolarization , membrane potential , chemistry , biophysics , repolarization , electrophysiology , neuroscience , biology
1 Whole‐cell recordings and fura‐2 measurements of cytoplasmic [Ca 2+ ] were made in depolarizing bipolar cells isolated from the retinae of goldfish. The aim was to study the voltage signal that regulates Ca 2+ influx in the synaptic terminal. 2 The current‐voltage relation was linear up to about −44 mV. At this threshold, the injection of 1 pA of current triggered a maintained ‘all‐or‐none’ depolarization to a plateau of −34 mV, associated with a decrease in input resistance and a damped voltage oscillation with a frequency of 50–70 Hz and initial amplitude of 4–10 mV. A second frequency component of 5–10 Hz was often observed. In a minority of cells the response to current injection was transient, recovering with an undershoot. 3 Unstimulated bipolar cells generated similar voltage signals, driven by current entering the cell through a non‐specific cation conductance that continuously varied in amplitude. 4 The threshold for activation of the Ca 2+ current was −43 mV and free [Ca 2+ ] i in the synaptic terminal rose during a depolarizing response. Simultaneous measurements of the fluorescence associated with the membrane marker FM1–43 demonstrated that these Ca 2+ signals stimulated exocytosis. Regenerative depolarizations and associated rises in [Ca 2+ ] i were blocked by inhibiting l ‐type Ca 2+ channels with 30 μ m nifedipine. 5 Depolarization beyond −40 mV also elicited an outwardly rectifying K + current. Blocking this current by replacing external Ca 2+ with Ba 2+ caused the voltage reached during a depolarizing response to increase to +10 mV. 6 The majority of the K + current was blocked by 100 n m charybdotoxin, indicating that it was carried by large‐conductance Ca 2+ ‐activated K + channels. A transient voltage‐gated K 2+ current remained, which began to activate at −40 mV. High‐frequency voltage oscillations were blocked by 100 n m charybdotoxin, but low‐frequency oscillations remained. 7 These results indicate that the voltage response of depolarizing bipolar cells is shaped by l ‐type Ca 2+ channels, Ca + ‐activated K + channels and voltage‐dependent K + channels. This combination of conductances regulates Ca 2+ influx into the synaptic terminal and confers an electrical resonance on the bipolar cell.