Spontaneous neurotransmission signals through store-driven Ca2+ transients to maintain synaptic homeostasis

Austin L. Reese, Ege T. Kavalali

Research output: Contribution to journalArticlepeer-review

50 Scopus citations


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.

Original languageEnglish (US)
Article numbere09262
Issue numberJULY2015
StatePublished - Jul 24 2015

ASJC Scopus subject areas

  • Neuroscience(all)
  • Immunology and Microbiology(all)
  • Biochemistry, Genetics and Molecular Biology(all)


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