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• W1763478481 abstract "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." @default.
• W1763478481 created "2016-06-24" @default.
• W1763478481 creator A5059395438 @default.
• W1763478481 creator A5063153560 @default.
• W1763478481 date "2015-07-24" @default.
• W1763478481 modified "2023-10-03" @default.
• W1763478481 title "Spontaneous neurotransmission signals through store-driven Ca2+ transients to maintain synaptic homeostasis" @default.
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• W1763478481 doi "https://doi.org/10.7554/elife.09262" @default.
• W1763478481 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4534843" @default.
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• W1763478481 hasPublicationYear "2015" @default.
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