HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) 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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Stuenkel, E L Articles by Nordmann, J J Search for Related Content PubMed PubMed Citation Articles by Stuenkel, E L Articles by Nordmann, J J

Department of Physiology, University of Michigan, Ann Arbor 48109-0622.

1. Monitoring of [Ca2+]i and vasopressin secretion in isolated nerve endings from the rat neurohypophysis were studied to determine the relationship between the time course of vasopressin secretion and depolarization-induced changes in [Ca2+]i. 2. Membrane depolarization by increasing the extracellular [K+] led to concentration-dependent, parallel increases in the amount of vasopressin release and in peak increases in [Ca2+]i. Half-maximal activation of a change in [Ca2+]i was attained at 40 mM extracellular K+. 3. The Ca2+ chelator dimethyl-BAPTA (1,2-bis(O-aminophenoxy)ethane-N,N,N'N'-tetraacetic acid), loaded into the nerve endings, reduced K+ depolarization-evoked vasopressin release and efficiently antagonized K(+)-induced changes in [Ca2+]i. Moreover, dimethyl-BAPTA dramatically reduced basal [Ca2+]i without a reduction in basal secretion. 4. The duration of the vasopressin secretory response was similar regardless of applied 50 mM K+ depolarizations longer than 30 s. The t1/2 of the secretory response was 45 s. Application of repetitive K+ depolarization pulses repetitive secretory responses of similar amplitude and duration. 5. The K(+)-induced changes in [Ca2+]i remained elevated throughout the duration of the depolarizing stimulus decreasing less than 30% over 3 min. The sustained increase in [Ca2+]i resulted largely from continued enhanced Ca2+ influx, demonstrated by susceptibility to the dihydropyridine, L-type calcium channel blocker, nicardipine. 6. Vasopressin secretion could be reinitiated following its decline to a step K+ depolarization by a further step increase in K+ or by removal and readdition of extracellular [Ca2+]. Alterations in [Ca2+]i paralleled periods of secretory activity. 7. Analysis of secretory responsiveness and change in [Ca2+]i to K+ depolarization in medium of altered extracellular [Ca2+] indicates that [Ca2+]i of 20 microM is sufficient to trigger vasopressin release. K(+)-induced alterations in [Ca2+]i could be observed at [Ca2+]o as low as 5 microM. Although smaller in amplitude to that observed at 2.2 mM [Ca2+]o the duration of the K(+)-induced secretory response increased at lower [Ca2+]o. 8. Transient vasopressin secretory responses were observed to sustained levels of [Ca2+] in digitonin and streptolysin-O-permeabilized nerve endings. Secretion could be re-evoked, following its decline, by a step increase in [Ca2+] or by removal and readdition of [Ca2+]o.(ABSTRACT TRUNCATED AT 400 WORDS)

This article has been cited by other articles:

				G. H. Kim, P. Kosterin, A. L. Obaid, and B. M. Salzberg A Mechanical Spike Accompanies the Action Potential in Mammalian Nerve Terminals Biophys. J., May 1, 2007; 92(9): 3122 - 3129. [Abstract] [Full Text] [PDF]

				B.-J. Zhang, K. Kusano, P. Zerfas, A. Iacangelo, W. S. Young III, and H. Gainer Targeting of Green Fluorescent Protein to Secretory Granules in Oxytocin Magnocellular Neurons and Its Secretion from Neurohypophysial Nerve Terminals in Transgenic Mice Endocrinology, March 1, 2002; 143(3): 1036 - 1046. [Abstract] [Full Text] [PDF]

				N. Hussy, V. Bres, M. Rochette, A. Duvoid, G. Alonso, G. Dayanithi, and F. C. Moos Osmoregulation of Vasopressin Secretion via Activation of Neurohypophysial Nerve Terminals Glycine Receptors by Glial Taurine J. Neurosci., September 15, 2001; 21(18): 7110 - 7116. [Abstract] [Full Text] [PDF]

				T. Sakaba and E. Neher Quantitative Relationship between Transmitter Release and Calcium Current at the Calyx of Held Synapse J. Neurosci., January 15, 2001; 21(2): 462 - 476. [Abstract] [Full Text] [PDF]

				M. Muschol and B. M. Salzberg Dependence of Transient and Residual Calcium Dynamics on Action-Potential Patterning during Neuropeptide Secretion J. Neurosci., September 15, 2000; 20(18): 6773 - 6780. [Abstract] [Full Text] [PDF]

				D. R. Giovannucci, M. D. Hlubek, and E. L. Stuenkel Mitochondria Regulate the Ca2+-Exocytosis Relationship of Bovine Adrenal Chromaffin Cells J. Neurosci., November 1, 1999; 19(21): 9261 - 9270. [Abstract] [Full Text] [PDF]

				S. Thirion, J.-D. Troadec, N. B. Pivovarova, S. Pagnotta, S. B. Andrews, R. D. Leapman, and G. Nicaise Stimulus-secretion coupling in neurohypophysial nerve endings: A role for intravesicular sodium? PNAS, March 16, 1999; 96(6): 3206 - 3210. [Abstract] [Full Text] [PDF]

				M. A. Bittner, V. G. Krasnoperov, E. L. Stuenkel, A. G. Petrenko, and R. W. Holz A Ca2+-Independent Receptor for alpha -Latrotoxin, CIRL, Mediates Effects on Secretion via Multiple Mechanisms J. Neurosci., April 15, 1998; 18(8): 2914 - 2922. [Abstract] [Full Text] [PDF]

				K. I. Rusin, D. R. Giovannucci, E. L. Stuenkel, and H. C. Moises kappa -Opioid Receptor Activation Modulates Ca2+ Currents and Secretion in Isolated Neuroendocrine Nerve Terminals J. Neurosci., September 1, 1997; 17(17): 6565 - 6574. [Abstract] [Full Text] [PDF]

				J. L. Branchaw, M. I. Banks, and M. B. Jackson Ca2+- and Voltage-Dependent Inactivation of Ca2+ Channels in Nerve Terminals of the Neurohypophysis J. Neurosci., August 1, 1997; 17(15): 5772 - 5781. [Abstract] [Full Text] [PDF]