Premium
Calcium‐induced calcium release in rod photoreceptor terminals boosts synaptic transmission during maintained depolarization
Author(s) -
Cadetti Lucia,
Bryson Eric J.,
Ciccone Cory A.,
Rabl Katalin,
Thoreson Wallace B.
Publication year - 2006
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2006.04845.x
Subject(s) - ryanodine receptor , depolarization , calcium , excitatory postsynaptic potential , neurotransmission , biophysics , ribbon synapse , chemistry , neuroscience , biology , synaptic vesicle , biochemistry , inhibitory postsynaptic potential , receptor , vesicle , organic chemistry , membrane
We examined the contribution of calcium‐induced calcium release (CICR) to synaptic transmission from rod photoreceptor terminals. Whole‐cell recording and confocal calcium imaging experiments were conducted on rods with intact synaptic terminals in a retinal slice preparation from salamander. Low concentrations of ryanodine stimulated calcium increases in rod terminals, consistent with the presence of ryanodine receptors. Application of strong depolarizing steps (−70 to −10 mV) exceeding 200 ms or longer in duration evoked a wave of calcium that spread across the synaptic terminals of voltage‐clamped rods. This secondary calcium increase was blocked by high concentrations of ryanodine, indicating it was due to CICR. Ryanodine (50 µ m ) had no significant effect on rod calcium current ( I ca ) although it slightly diminished rod light‐evoked voltage responses. Bath application of 50 µ m ryanodine strongly inhibited light‐evoked currents in horizontal cells. Whether applied extracellularly or delivered into the rod cell through the patch pipette, ryanodine (50 µ m ) also inhibited excitatory post‐synaptic currents (EPSCs) evoked in horizontal cells by depolarizing steps applied to rods. Ryanodine caused a preferential reduction in the later portions of EPSCs evoked by depolarizing steps of 200 ms or longer. These results indicate that CICR enhances calcium increases in rod terminals evoked by sustained depolarization, which in turn acts to boost synaptic exocytosis from rods.