Literature DB >> 19158310

F-actin and myosin II accelerate catecholamine release from chromaffin granules.

Khajak Berberian1, Alexis J Torres, Qinghua Fang, Kassandra Kisler, Manfred Lindau.   

Abstract

The roles of nonmuscle myosin II and cortical actin filaments in chromaffin granule exocytosis were studied by confocal fluorescence microscopy, amperometry, and cell-attached capacitance measurements. Fluorescence imaging indicated decreased mobility of granules near the plasma membrane following inhibition of myosin II function with blebbistatin. Slower fusion pore expansion rates and longer fusion pore lifetimes were observed after inhibition of actin polymerization using cytochalasin D. Amperometric recordings revealed increased amperometric spike half-widths without change in quantal size after either myosin II inhibition or actin disruption. These results suggest that actin and myosin II facilitate release from individual chromaffin granules by accelerating dissociation of catecholamines from the intragranular matrix possibly through generation of mechanical forces.

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Year:  2009        PMID: 19158310      PMCID: PMC2768403          DOI: 10.1523/JNEUROSCI.2818-08.2009

Source DB:  PubMed          Journal:  J Neurosci        ISSN: 0270-6474            Impact factor:   6.167


  43 in total

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  54 in total

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Review 8.  The fusion pore, 60 years after the first cartoon.

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9.  Huntingtin-associated protein 1 regulates exocytosis, vesicle docking, readily releasable pool size and fusion pore stability in mouse chromaffin cells.

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10.  The neuronal calcium sensor Synaptotagmin-1 and SNARE proteins cooperate to dilate fusion pores.

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