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Journal of Neuroscience, Vol 16, 1370-1379, Copyright © 1996 by Society for Neuroscience

ARTICLE

Ba2+ ions evoke two kinetically distinct patterns of exocytosis in chromaffin cells, but not in neurohypophysial nerve terminals

EP Seward, NI Chernevskaya and MC Nowycky
Department of Neurobiology and Anatomy, Medical College of Pennsylvania, Philadelphia 19129, USA.

The coupling between divalent cations and exocytosis of large dense- cored vesicles (LDCV) was studied with capacitance-detection techniques in nerve terminals of the rat neurohypophysis (NHP) and bovine chromaffin cells. Ba2+ substitution for Ca2+ produced kinetically distinct responses in the two preparations. In NHP terminals, Ba2+ ions behave as weak substitutes for Ca2+. Exocytotic events occur principally during depolarizing pulses, i.e., events are "stimulus- coupled" to Ba2+ entry through voltage-gated Ca2+ channels. Stimulus- coupled exocytosis apparently requires elevated submembrane cation concentrations that dissipate rapidly on hyperpolarization-induced Ca(2+)-channel closure. Intracellular dialysis of NHP terminals with Ba2+ does not evoke exocytosis, nor does it interfere with depolarization-evoked Ca2+ influx and exocytosis. In chromaffin cells, Ba2+ ions evoke a small quantity of stimulus-coupled secretion, but the dominant response is an additional pronounced poststimulus capacitance increase that outlasts channel closures by 20-50 sec. "Stimulus- decoupled" exocytosis is slow (approximately 25-40 fF/sec) compared with Ca(2+)-evoked stimulus-coupled exocytosis (approximately 1000 fF/sec). Decoupled secretion is not attributable to Ba2+ displacement of intracellular Ca2+ ions, because it is insensitive to 10 mM EGTA or thapsigargin. Slow exocytosis is initiated by inclusion of Ba2+ ions in the recording pipette and continues steadily for 5-12 min, producing a total increase of several thousand fF, which ultimately doubles or triples the original cell-surface area. We propose that two pathways of regulated exocytosis with distinct kinetics and divalent cation sensitivity exist in chromaffin cells. Only a single kinetic pattern is detected in NHP terminals, suggesting that mechanisms for secretion are not universally distributed in excitable cells.

This article has been cited by other articles:

				C. S. Bauer, R. J. Woolley, A. G. Teschemacher, and E. P. Seward Potentiation of Exocytosis by Phospholipase C-Coupled G-Protein-Coupled Receptors Requires the Priming Protein Munc13-1 J. Neurosci., January 3, 2007; 27(1): 212 - 219. [Abstract] [Full Text] [PDF]

				R. Thiagarajan, J. Wilhelm, T. Tewolde, Y. Li, M. M. Rich, and K. L. Engisch Enhancement of Asynchronous and Train-Evoked Exocytosis in Bovine Adrenal Chromaffin Cells Infected With a Replication Deficient Adenovirus J Neurophysiol, November 1, 2005; 94(5): 3278 - 3291. [Abstract] [Full Text] [PDF]

				A. G. Teschemacher and E. P. Seward Bidirectional Modulation of Exocytosis by Angiotensin II Involves Multiple G-Protein-Regulated Transduction Pathways in Chromaffin Cells J. Neurosci., July 1, 2000; 20(13): 4776 - 4785. [Abstract] [Full Text] [PDF]

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