Calcium regulation of spontaneous and asynchronous neurotransmitter release

Stephen M. Smith, Wenyan Chen, Nicholas P. Vyleta, Courtney Williams, Chia Hsueh Lee, Cecilia Phillips, Michael C. Andresen

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


The molecular machinery underlying action potential-evoked, synchronous neurotransmitter release, has been intensely studied. It was presumed that two other forms of exocytosis, delayed (asynchronous) and spontaneous transmission, were mediated by the same voltage-activated Ca2+ channels (VACCs), intracellular Ca2+ sensors and vesicle pools. However, a recent explosion in the study of spontaneous and asynchronous release has shown these presumptions to be incorrect. Furthermore, the finding that different forms of synaptic transmission may mediate distinct physiological functions emphasizes the importance of identifying the mechanisms by which Ca2+ regulates spontaneous and asynchronous release. In this article, we will briefly summarize new and published data on the role of Ca2+ in regulating spontaneous and asynchronous release at a number of different synapses. We will discuss how an increase of extracellular [Ca2+] increases spontaneous and asynchronous release, show that VACCs are involved at only some synapses, and identify regulatory roles for other ion channels and G protein-coupled receptors. In particular, we will focus on two novel pathways that play important roles in the regulation of non-synchronous release at two exemplary synapses: one modulated by the Ca2+-sensing receptor and the other by transient receptor potential cation channel sub-family V member 1.

Original languageEnglish (US)
Pages (from-to)226-233
Number of pages8
JournalCell Calcium
Issue number3-4
StatePublished - Sep 2012


  • Calcium channel
  • Calcium-sensing receptor
  • Spontaneous release
  • Synchronous release
  • VACC

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology


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