Abstract
The mechanisms of release, depletion, and refilling of endoplasmic reticulum (ER) Ca2+ were investigated in type I horizontal cells of the carp retina using a fluo-3-based Ca2+ imaging technique. Exogenous application of caffeine, a ryanodine receptor agonist, induced oscillatory intracellular free Ca2+ concentration ([Ca2+]i) responses in a duration- and concentration-dependent manner. In Ca2+-free Ringer’s solution, [Ca2+]i transients could also be induced by a brief caffeine application, whereas subsequent caffeine application induced no [Ca2+]i increase, which implied that extracellular Ca2+ was required for ER refilling, confirming the necessity of a Ca2+ influx pathway for ER refilling. Depletion of ER Ca2+ by thapsigargin triggered a Ca2+ influx which could be blocked by the store-operated channel inhibitor 2-APB, which proved the existence of the store-operated Ca2+ entry pathway. Taken together, these results suggested that after being depleted by caffeine, the ER was replenished by Ca2+ influx via store-operated channels. These results reveal the fine modulation of ER Ca2+ signaling, and the activation of the store-operated Ca2+ entry pathway guarantees the replenishment of the ER so that the cell can be ready for response to the subsequent stimulus.
Highlights
Ca2+ is a ubiquitous intracellular messenger that regulates numerous cellular processes including muscle contraction, transmitter release, apoptosis, and so on [1,2]
The basic findings are: (1) caffeine induced oscillatory [Ca2+]i responses in a duration- and concentration-dependent manner, (2) removal of extracellular Ca2+ abolished the repeatability of caffeineinduced [Ca2+]i responses, (3) inhibition of L-type voltage-gated Ca2+ channels (L-VGCCs) reduced caffeine-induced [Ca2+]i oscillations, (4) inhibition of store-operated channels (SOCs) abolished caffeine-induced [Ca2+]i oscillations. These results reveal the fine modulation of endoplasmic reticulum (ER) Ca2+ signaling, and the activation of the store-operated Ca2+ entry (SOCE) pathway guarantees the replenishment of the ER so that the cell can be ready for response to the subsequent stimulus
We investigated the mechanisms of release, depletion, and refilling of ER Ca2+ in carp retinal HCs
Summary
Ca2+ is a ubiquitous intracellular messenger that regulates numerous cellular processes including muscle contraction, transmitter release, apoptosis, and so on [1,2]. When activated by proper stimulation, the opening of the plasma membrane Ca2+ channels or the activation of Ca2+ release channels on the intracellular Ca2+ stores (largely the endoplasmic reticulum, ER) leads to the elevation of [Ca2+]i [2]. As the primary intracellular reservoir of Ca2+ and a major source of [Ca2+]i elevation, the ER is involved in a wide range of neuronal Ca2+-dependent processes, such as synaptic transmission and plasticity [4,5]. The ER accumulates Ca2+ by active transport of Ca2+ from the cytoplasm into the ER by Ca2+-ATPase (sarco/ endoplasmic reticulum Ca2+-ATPase, SERCA) pumps expressed on the ER membrane. While IP3Rs are gated by IP3, both IP3Rs and RyRs can be activated by Ca2+, and such Ca2+-induced Ca2+
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