Secretagogue stimulation of neurosecretory cells elicits filopodial extensions uncovering new functional release sites

Papadopulos, Andreas, Martin, Sally, Tomatis, Vanesa M., Gormal, Rachel S. and Meunier, Frederic A. (2013) Secretagogue stimulation of neurosecretory cells elicits filopodial extensions uncovering new functional release sites. Journal of Neuroscience, 33 49: 19143-19153. doi:10.1523/JNEUROSCI.2634-13.2013

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Author Papadopulos, Andreas
Martin, Sally
Tomatis, Vanesa M.
Gormal, Rachel S.
Meunier, Frederic A.
Title Secretagogue stimulation of neurosecretory cells elicits filopodial extensions uncovering new functional release sites
Journal name Journal of Neuroscience   Check publisher's open access policy
ISSN 0270-6474
1563-5279
Publication date 2013
Year available 2013
Sub-type Article (original research)
DOI 10.1523/JNEUROSCI.2634-13.2013
Open Access Status File (Publisher version)
Volume 33
Issue 49
Start page 19143
End page 19153
Total pages 11
Place of publication London, United Kingdom
Publisher Informa Healthcare
Collection year 2014
Language eng
Subject 2800 Neuroscience
Abstract Regulated exocytosis in neurosecretory cells relies on the timely fusion of secretory granules (SGs) with the plasma membrane. Secretagogue stimulation leads to an enlargement of the cell footprint (surface area in contact with the coverslip), an effect previously attributed to exocytic fusion of SGs with the plasma membrane. Using total internal reflection fluorescence microscopy, we reveal the formation of filopodia-like structures in bovine chromaffin and PC12 cells driving the footprint expansion, suggesting the involvement of cortical actin network remodeling in this process. Using exocytosis-incompetent PC12 cells, we demonstrate that footprint enlargement is largely independent of SG fusion, suggesting that vesicular exocytic fusion plays a relatively minor role in filopodial expansion. The footprint periphery, including filopodia, undergoes extensive F-actin remodeling, an effect abolished by the actomyosin inhibitors cytochalasin D and blebbistatin. Imaging of both Lifeact-GFP and the SG marker protein neuropeptide Y-mCherry reveals that SGs actively translocate along newly forming actin tracks before undergoing fusion. Together, these data demonstrate that neurosecretory cells regulate the number of SGs undergoing exocytosis during sustained stimulation by controlling vesicular mobilization and translocation to the plasma membrane through actin remodeling. Such remodeling facilitates the de novo formation of fusion sites.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Queensland Brain Institute Publications
Official 2014 Collection
 
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Citation counts: TR Web of Science Citation Count  Cited 10 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 11 times in Scopus Article | Citations
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