Endogenous calcium buffering at photoreceptor synaptic terminals in salamander retina

Calcium operates by several mechanisms to regulate glutamate release at rod and cone synaptic terminals. In addition to serving as the exocytotic trigger, Ca 2+ accelerates replenishment of vesicles in cones and triggers Ca 2+ ‐induced Ca 2+ release (CICR) in rods. Ca 2+ thereby amplifies sustained exocytosis, enabling photoreceptor synapses to encode constant and changing light. A complete picture of the role of Ca 2+ in regulating synaptic transmission requires an understanding of the endogenous Ca 2+ handling mechanisms at the synapse. We therefore used the “added buffer” approach to measure the endogenous Ca 2+ binding ratio ( κ endo ) and extrusion rate constant ( γ ) in synaptic terminals of photoreceptors in retinal slices from tiger salamander. We found that κ endo was similar in both cell types—∼25 and 50 in rods and cones, respectively. Using measurements of the decay time constants of Ca 2+ transients, we found that γ was also similar, with values of ∼100 s −1 and 160 s −1 in rods and cones, respectively. The measurements of κ endo differ considerably from measurements in retinal bipolar cells, another ribbon‐bearing class of retinal neurons, but are comparable to similar measurements at other conventional synapses. The values of γ are slower than at other synapses, suggesting that Ca 2+ ions linger longer in photoreceptor terminals, supporting sustained exocytosis, CICR, and Ca 2+ ‐dependent ribbon replenishment. The mechanisms of endogenous Ca 2+ handling in photoreceptors are thus well‐suited for supporting tonic neurotransmission. Similarities between rod and cone Ca 2+ handling suggest that neither buffering nor extrusion underlie differences in synaptic transmission kinetics. Synapse 68:518–528, 2014 . © 2014 Wiley Periodicals, Inc.