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This Article Full Text Full Text (PDF) All Versions of this Article: 585/3/655    most recent jphysiol.2007.136135v1 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 Vardjan, N. Articles by Zorec, R. Search for Related Content PubMed PubMed Citation Articles by Vardjan, N. Articles by Zorec, R. Related Collections Review articles

Nina Vardjan^1,2, Matja Stenovec^1,2, Jernej Jorgaevski², Marko Kreft^2,1 and Robert Zorec^2,1

¹ Celica Biomedical Center, LCI, Proletarska cesta 4, 1000 Ljubljana, Slovenia
² LN-MCP, Institute of Pathophysiology, Faculty of Medicine, University of Ljubljana, Zaloka 4, 1000 Ljubljana, Slovenia

The release of hormones and neurotransmitters by regulated exocytosis requires the delivery of secretory vesicles to the plasma membrane, where they dock and become primed for fusion with the plasma membrane. Upon stimulation a fusion pore is formed through which cargo molecules diffuse out of the vesicle lumen into the extracellular space. After the cargo release the fusion pore either closes (kiss-and-run, transient exocytosis), fluctuates between an open and a closed state (for short times, fusion pore flickering, or for rather longer periods, ‘pulsing pore’) or expands irreversibly (full fusion exocytosis). In almost all secretory cells spontaneous secretion of vesicle cargo can be detected in the absence of stimulation. Spontaneous and stimulated exocytosis were thought to exhibit similar properties at elementary level, differing only in the probability of occurrence. However, recent studies indicate that spontaneous exocytosis differs from the stimulated one in many respects, therefore opening questions about the physiological role of spontaneous exocytosis. In this report we address the elementary properties of spontaneous and stimulated peptidergic vesicle discharge which appears to be modulated by fusion pore conductance (diameter) and fusion pore gating.

(Received 10 May 2007; accepted after revision 4 June 2007; first published online 7 June 2007)
Corresponding author R. Zorec: University of Ljubljana, Faculty of Medicine, Institute of Pathophysiology, LN-MCP, Zaloka 4, 1000 Ljubljana, Slovenia. Email: robert.zorec{at}mf.uni-lj.si

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