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The Journal of Neuroscience, July 7, 2004, 24(27):6127-6132; doi:10.1523/JNEUROSCI.1563-04.2004
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Synaptotagmin I Synchronizes Transmitter Release in Mouse Hippocampal Neurons
Tei-ichi Nishiki andGeorge J. Augustine Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710
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.
Key words: synaptic transmission; synaptic vesicle; calcium; exocytosis; endocytosis; FM 4-64
Received April 23, 2004; revised May 26, 2004; accepted May 26, 2004.
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