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Front Cell Neurosci. 2014 Feb 3;8:20. doi: 10.3389/fncel.2014.00020. eCollection 2014.

Intracellular calcium stores drive slow non-ribbon vesicle release from rod photoreceptors.

Author information

1
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center Omaha, NE, USA ; Department of Ophthalmology and Visual Sciences, University of Nebraska Medical Center Omaha, NE, USA.
2
Department of Ophthalmology and Visual Sciences, Moran Eye Center, University of Utah School of Medicine Salt Lake City, UT, USA.

Abstract

Rods are capable of greater slow release than cones contributing to overall slower release kinetics. Slow release in rods involves Ca(2+)-induced Ca(2+) release (CICR). By impairing release from ribbons, we found that unlike cones where release occurs entirely at ribbon-style active zones, slow release from rods occurs mostly at ectopic, non-ribbon sites. To investigate the role of CICR in ribbon and non-ribbon release from rods, we used total internal reflection fluorescence microscopy as a tool for visualizing terminals of isolated rods loaded with fluorescent Ca(2+) indicator dyes and synaptic vesicles loaded with dextran-conjugated pH-sensitive rhodamine. We found that rather than simply facilitating release, activation of CICR by ryanodine triggered release directly in rods, independent of plasma membrane Ca(2+) channel activation. Ryanodine-evoked release occurred mostly at non-ribbon sites and release evoked by sustained depolarization at non-ribbon sites was mostly due to CICR. Unlike release at ribbon-style active zones, non-ribbon release did not occur at fixed locations. Fluorescence recovery after photobleaching of endoplasmic reticulum (ER)-tracker dye in rod terminals showed that ER extends continuously from synapse to soma. Release of Ca(2+) from terminal ER by lengthy depolarization did not significantly deplete Ca(2+) from ER in the perikaryon. Collectively, these results indicate that CICR-triggered release at non-ribbon sites is a major mechanism for maintaining vesicle release from rods and that CICR in terminals may be sustained by diffusion of Ca(2+) through ER from other parts of the cell.

KEYWORDS:

calcium-induced calcium release; exocytosis; retina; ribbon synapse; ryanodine receptors; synaptic vesicle; total internal reflection fluorescence microscopy

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