Roles of calmodulin and calmodulin-binding proteins in synaptic vesicle recycling during regulated exocytosis at submicromolar Ca2+ concentrations

Michihiro Igarashi, Michitoshi Watanabe

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)

Abstract

Calcium ion is required at various concentrations for vesicular recycling in the presynaptic terminal. Although calmodulin (CaM) is the most abundant Ca2+-binding protein and has a submicromolar affinity for Ca2+, it is not the Ca2+ sensor for vesicular fusion because this process requires Ca2+ concentrations above 1 μM. Several lines of evidence, however, suggest that CaM mediates the regulation of vesicular recycling by submicromolar Ca2+ via novel protein-protein interactions. In this review, we discuss recent findings on how CaM regulates synaptic vesicle recycling by controlling the SNARE mechanism, which is the molecular machinery that mediates exocytosis.

Original languageEnglish
Pages (from-to)226-233
Number of pages8
JournalNeuroscience Research
Volume58
Issue number3
DOIs
Publication statusPublished - 2007 Jul
Externally publishedYes

Keywords

  • CaMKII
  • Calcium
  • Calmodulin
  • Exocytosis
  • Myosin-V
  • Recycling
  • SNARE mechanism

ASJC Scopus subject areas

  • Neuroscience(all)

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