Journal
JOURNAL OF NEUROSCIENCE
Volume 24, Issue 27, Pages 6127-6132Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1563-04.2004
Keywords
synaptic transmission; synaptic vesicle; calcium; exocytosis; endocytosis; FM 4-64
Categories
Funding
- NIMH NIH HHS [R01 MH067044, MH-67044] Funding Source: Medline
- NINDS NIH HHS [R01 NS021624, NS-21624] Funding Source: Medline
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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.
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