Neurohormone Secretion Persists after Post-Afterdischarge Membrane Depolarization and Cytosolic Calcium Elevation in Peptidergic Neurons in Intact Nervous Tissue

Abstract

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.