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We have utilized the Ca2+ indicator dye, Arsenazo III, to examine the role of presynaptic Ca2+ concentration in two types of synaptic plasticity observed at the synapses of cell L10 in Aplysia californica; post-tetanic potentiation (p.t.p. - the increased transmitter release which follows high frequency stimulation), and resting membrane potential modulation of release. Intracellular Ca2+ was monitored in the cell body and main neurites of L10 injected with Arsenazo III. Tetanic stimulation caused an increase in intracellular Ca2+ concentration that decayed, after tetanus, with fast and slow time constants which paralleled the time course of decay of p.t.p. When the voltage-sensitive Ca2+ current was reduced by removing external Ca2+ (0 mM-Ca2+, 4 mM-EGTA) or by blocking Ca2+ channels with divalent cation channel blocker (4 mM-Cd2+), tetanic stimulation did not cause increases in Arsenazo absorbance even when Na+ currents were not blocked. This finding suggests that Ca2+ entering the cell through voltage-dependent Ca2+ channels was the major source of Ca2+ which accumulated during the tetanus. Transmitter release is increased when L10 is maintained at a depolarized membrane potential, and is decreased when L10 is hyperpolarized. We found that the base-line Arsenazo absorbance signal in L10 increased when L10 was depolarized from -60 to -40 mV and decreased when L10 was hyperpolarized. This finding supports the idea that the steady-state Ca2+ concentration contributes to the membrane-potential modulation of transmitter release. These results support the idea that transmitter release can be modulated by the residual or resting Ca2+ concentration of the presynaptic cell.

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