| First Author | Nishiki T | Year | 2004 |
| Journal | J Neurosci | Volume | 24 |
| Issue | 27 | Pages | 6127-32 |
| PubMed ID | 15240804 | Mgi Jnum | J:97274 |
| Mgi Id | MGI:3575070 | Doi | 10.1523/JNEUROSCI.1563-04.2004 |
| Citation | Nishiki T, et al. (2004) Synaptotagmin I synchronizes transmitter release in mouse hippocampal neurons. J Neurosci 24(27):6127-32 |
| abstractText | 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. |
