TY - JOUR TI - Spontaneous neurotransmission signals through store-driven Ca2+ transients to maintain synaptic homeostasis AU - Reese, Austin L AU - Kavalali, Ege T A2 - Raman, Indira M VL - 4 PY - 2015 DA - 2015/07/24 SP - e09262 C1 - eLife 2015;4:e09262 DO - 10.7554/eLife.09262 UR - https://doi.org/10.7554/eLife.09262 AB - Spontaneous glutamate release-driven NMDA receptor activity exerts a strong influence on synaptic homeostasis. However, the properties of Ca2+ signals that mediate this effect remain unclear. Here, using hippocampal neurons labeled with the fluorescent Ca2+ probes Fluo-4 or GCAMP5, we visualized action potential-independent Ca2+ transients in dendritic regions adjacent to fluorescently labeled presynaptic boutons in physiological levels of extracellular Mg2+. These Ca2+ transients required NMDA receptor activity, and their propensity correlated with acute or genetically induced changes in spontaneous neurotransmitter release. In contrast, they were insensitive to blockers of AMPA receptors, L-type voltage-gated Ca2+ channels, or group I mGluRs. However, inhibition of Ca2+-induced Ca2+ release suppressed these transients and elicited synaptic scaling, a process which required protein translation and eukaryotic elongation factor-2 kinase activity. These results support a critical role for Ca2+-induced Ca2+ release in amplifying NMDA receptor-driven Ca2+ signals at rest for the maintenance of synaptic homeostasis. KW - spontaneous neurotransmitter release KW - NMDA receptor signaling KW - Ca2+ induced Ca2+ release KW - homeostatic plasticity JF - eLife SN - 2050-084X PB - eLife Sciences Publications, Ltd ER -