Abstract
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 language | English |
|---|---|
| Pages (from-to) | 6127-6132 |
| Number of pages | 6 |
| Journal | Journal of Neuroscience |
| Volume | 24 |
| Issue number | 27 |
| DOIs | |
| Publication status | Published - Jul 7 2004 |
| Externally published | Yes |
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Keywords
- Calcium
- Endocytosis
- Exocytosis
- FM 4-64
- Synaptic transmission
- Synaptic vesicle
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Synaptotagmin I synchronizes transmitter release in mouse hippocampal neurons. / Nishiki, Tei-ichi; Augustine, George J.
In: Journal of Neuroscience, Vol. 24, No. 27, 07.07.2004, p. 6127-6132.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Synaptotagmin I synchronizes transmitter release in mouse hippocampal neurons
AU - Nishiki, Tei-ichi
AU - Augustine, George J.
PY - 2004/7/7
Y1 - 2004/7/7
N2 - 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.
AB - 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.
KW - Calcium
KW - Endocytosis
KW - Exocytosis
KW - FM 4-64
KW - Synaptic transmission
KW - Synaptic vesicle
UR - http://www.scopus.com/inward/record.url?scp=3042796387&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3042796387&partnerID=8YFLogxK
U2 - 10.1523/JNEUROSCI.1563-04.2004
DO - 10.1523/JNEUROSCI.1563-04.2004
M3 - Article
C2 - 15240804
AN - SCOPUS:3042796387
VL - 24
SP - 6127
EP - 6132
JO - Journal of Neuroscience
JF - Journal of Neuroscience
SN - 0270-6474
IS - 27
ER -