The purpose of this work was to test the hypothesis that an electrical afterdischarge (AD) causes prolonged elevation in cytosolic calcium levels that is associated with prolonged secretion of egg-laying hormone (ELH) from peptidergic neurons in intact nervous tissue of Aplysia. Using a combination of radioimmunoassay measurement of ELH secretion, electrophysiological measurement of membrane potential, and optical imaging of the concentration of intracellular free calcium ions ([Ca2+]i), we verified that there was persistent secretion of ELH after the end of the AD; this was accompanied by prolonged post-AD membrane depolarization and prolonged post-AD elevation in [Ca2+]i. Extracellular treatment with the calcium chelator EGTA had no effect on the pattern or magnitude of ELH secretion or on the post-AD membrane potential (V(m)) and post-AD Ca2+ signal, ruling out a role for extracellular calcium in the post-AD elevation of [Ca2+]i. Both V(m) and [Ca2+]i returned to baseline well before ELH secretion, such that neither prolonged membrane depolarization nor prolonged Ca2+ signaling can fully account for the extent of the persistent secretion of ELH. These findings suggest a unique relationship between membrane excitability, Ca2+ signaling, and prolonged neuropeptide secretion.
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Michel et al. (2002) studied this question.
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