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

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

Blog Article

Rods are capable of greater slow release than cones contributing to overall slower release kinetics.Slow release in rods involves Ca2+-induced Ca2+ 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 (TIRFM) as a tool for visualizing terminals of isolated rods loaded with fluorescent Ca2+ indicator dyes and synaptic vesicles loaded with dextran-conjugated pH-sensitive rhodamine (pHrodo).We found that rather than Side Table simply facilitating release, activation of CICR by ryanodine triggered release directly in rods, independent of plasma membrane Ca2+ 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 Ca2+ from terminal ER by lengthy depolarization did not significantly deplete Ca2+ from ER in the perikaryon.Collectively, these results indicate that CICR-triggered release at non-ribbon sites Snap Caps is a major mechanism for maintaining vesicle release from rods and that CICR in terminals may be sustained by diffusion of Ca2+ through ER from other parts of the cell.