Ca2+ Diffusion through Endoplasmic Reticulum Supports Elevated Intraterminal Ca2+ Levels Needed to Sustain Synaptic Release from Rods in Darkness

• DOI: 10.1523/jneurosci.0754-15.2015
• Publication Date: 2015-08-12T16:29:42Z
• Authors: M. Chen; M. J. Van Hook; W. B. Thoreson
• Keywords: Darkness

In addition to vesicle release at synaptic ribbons, rod photoreceptors are capable of substantial slow non-ribbon sites triggered by Ca²⁺-induced Ca²⁺ (CICR) from intracellular stores. To maintain CICR as rods remain depolarized in darkness, we hypothesized that released into the cytoplasm terminal endoplasmic reticulum (ER) can be replenished continuously ions diffusing within ER soma. We measured [Ca²⁺] changes and <i>Ambystoma tigrinum</i> retina using various dyes. were loading with fluo-5N then washing dye a dye-free patch pipette solution. Small molecules diffused between soma showing single continuous compartment. Depolarization −40 mV depleted ER, followed decline somatic [Ca²⁺]. Local activation ryanodine receptors terminals spatially confined puff caused [Ca²⁺], secondary decrease ER. Localized photolytic uncaging <i>o</i>-nitrophenyl-EGTA an abrupt increase slower These data suggest that, during maintained depolarization, soma-to-terminal gradient develops promotes diffusion resupply intraterminal stores thus sustain CICR-mediated release. The ability move freely through may also promote bidirectional communication terminal. <b>SIGNIFICANCE STATEMENT</b> Vertebrate cone both vesicles but exhibit (CICR). Blocking inhibits &gt;50% darkness. How do sufficiently high support sustained CICR-driven transmission? show depolarization creates lumen replenish This mechanism allows CICR-triggered indefinitely while Free communicate back influence other critical cell processes.