Kinetic efficiency of endocytosis at mammalian CNS synapses requires synaptotagmin I Academic Article uri icon


MeSH Major

  • Calcium-Binding Proteins
  • Endocytosis
  • Membrane Glycoproteins
  • Nerve Tissue Proteins
  • Synapses


  • At nerve terminals, synaptic vesicle components are retrieved from the cell surface and recycled for local reuse soon after exocytosis. The kinetics of this coupling is critical for the proper functioning of synapses during repetitive action potential firing, because deficiencies in this process lead to abnormal depletion of the releasable vesicle pool. Although the molecular basis of this coupling is poorly understood, numerous biochemical data point to a role for synaptotagmin I (SytI), an essential synaptic vesicle protein required for fast calcium-dependent exocytosis. Here, using synapto-pHluorin in an approach that allows the dissection of endocytosis and exocytosis into separate components during periods of stimulation, we examined exocytic-endocytic coupling in synapses from SytI knockout mice and their WT littermates. We show that endocytosis is significantly impaired in the absence of SytI with the relative rates of endocytosis compared with exocytosis reduced approximately 3-fold with respect to WT. Thus, in addition to regulating exocytosis, SytI also controls the kinetic efficiency of endocytosis at nerve terminals.

publication date

  • November 23, 2004



  • Academic Article



  • eng

PubMed Central ID

  • PMC534526

Digital Object Identifier (DOI)

  • 10.1073/pnas.0406968101

PubMed ID

  • 15492212

Additional Document Info

start page

  • 16648

end page

  • 52


  • 101


  • 47