This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wayne, N. L. Articles by de Quintana, S. B. Search for Related Content PubMed PubMed Citation Articles by Wayne, N. L. Articles by de Quintana, S. B.

Post-Afterdischarge Depolarization Does Not Stimulate Prolonged Neurohormone Secretion but Is Required for Activity-Dependent Stimulation of Neurohormone Biosynthesis from Peptidergic Neurons

Department of Physiology, David Geffen School of Medicine at University of California-Los Angeles, Los Angeles, California 90095-1751

Address all correspondence and requests for reprints to: Nancy L. Wayne, Department of Physiology, Room 53-231, Center for Health Sciences, David Geffen School of Medicine at University of California-Los Angeles, 10833 Le Conte Avenue, Los Angeles, California 90095-1751. E-mail: nwayne{at}mednet.ucla.edu.

Membrane depolarization plays a critical role in stimulating secretion of neuropeptides and can also be important in regulating transcriptional and translational events that control peptide biosynthesis. The purpose of this study was to test the hypothesis that persistent membrane depolarization after the end of an electrical afterdischarge plays an important role in stimulating both prolonged secretion of egg-laying hormone (ELH) and ELH synthesis from peptidergic bag cell neurons of Aplysia. Experimental preparations were treated with a low Na⁺ solution to rapidly repolarize membrane potential (Vm). Compared with control preparations, the low Na⁺ solution caused rapid membrane repolarization to resting levels, significant shortening of the duration of the afterdischarge, and significant decrease in the decay time constant of cytosolic Ca²⁺ ([Ca²⁺]_i) concentrations, but no effect on peak [Ca²⁺]_i, total [Ca²⁺]_i above baseline, or duration of elevated [Ca²⁺]_i. Contrary to both theoretical expectations and findings in other cell types, low Na⁺ treatment and the resulting premature repolarization of Vm did not inhibit ELH secretion. On the other hand, low Na⁺ treatment that blocked prolonged depolarization, as well as inhibition of Ca²⁺ influx, prevented the afterdischarge-induced stimulation of ELH synthesis. These findings provide support for membrane depolarization acting as a trigger mechanism, rather than a sustained driving force, for cellular events that control ELH secretion. It also demonstrates, for the first time, a critical role for postdischarge Vm in regulating an important aspect of neuroendocrine cell function—that of hormone synthesis.

This article has been cited by other articles:

				J. E. Geiger and N. S. Magoski Ca2+-Induced Ca2+ Release in Aplysia Bag Cell Neurons Requires Interaction Between Mitochondrial and Endoplasmic Reticulum Stores J Neurophysiol, July 1, 2008; 100(1): 24 - 37. [Abstract] [Full Text] [PDF]