Calcium levels measured in a presynaptic neurone of Aplysia under conditions that modulate transmitter release.

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Abstract
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.