Synaptotagmin I synchronizes transmitter release in mouse hippocampal neurons

Tei Ichi Nishiki, George J. Augustine

Research output: Contribution to journalArticlepeer-review

134 Citations (Scopus)


We have asked whether loss of the Ca2+ sensor protein synaptotagmin I influences the total amount of neurotransmitter released after a presynaptic action potential. Hippocampal neurons from synaptotagmin I knock-out mice had a greatly reduced fast synchronous component of glutamate release, as reported previously. However, the amount of glutamate released during the slow asynchronous component increased in these knock-out neurons. As a result of these changes in the kinetics of release, there was no significant difference between wild-type and knock-out neurons in the total amount of transmitter released within 400 msec after a presynaptic stimulus. Fluorescence imaging experiments demonstrated that wild-type and knock-out neurons take up and release similar amounts of FM dye after depolarization, indicating normal amounts of synaptic vesicle trafficking in the knock-out neurons. These results indicate that synaptotagmin I knock-out neurons are fully capable of releasing neurotransmitter, with the increased slow component of release serving to compensate for loss of the fast component. Thus, synaptotagmin I synchronizes the rapid release of neurotransmitters after Ca2+ entry into presynaptic terminals and also appears to suppress the slower, asynchronous form of transmitter release.

Original languageEnglish
Pages (from-to)6127-6132
Number of pages6
JournalJournal of Neuroscience
Issue number27
Publication statusPublished - Jul 7 2004
Externally publishedYes


  • Calcium
  • Endocytosis
  • Exocytosis
  • FM 4-64
  • Synaptic transmission
  • Synaptic vesicle

ASJC Scopus subject areas

  • Neuroscience(all)


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