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Spontaneous glutamate release-driven NMDA receptor activity exerts a strong influence on synaptic homeostasis. However, the properties of Ca 2+  signals that mediate this effect remain unclear. Here, using hippocampal neurons labeled with the fluorescent Ca 2+  probes Fluo-4 or GCAMP5, we visualized action potential-independent Ca 2+  transients in dendritic regions adjacent to fluorescently labeled presynaptic boutons in physiological levels of extracellular Mg 2+ . These Ca 2+  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 Ca 2+  channels, or group I mGluRs. However, inhibition of Ca 2+ -induced Ca 2+  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 Ca 2+ -induced Ca 2+  release in amplifying NMDA receptor-driven Ca 2+  signals at rest for the maintenance of synaptic homeostasis.

Spontaneous neurotransmission signals through store-driven Ca 2+ transients to maintain synaptic homeostasis