Abstract
Neurotransmitter release proceeds by Ca2+-triggered, SNARE-complex-dependent synaptic vesicle fusion. After fusion, the ATPase NSF and its cofactors α- and βSNAP disassemble SNARE complexes, thereby recycling individual SNAREs for subsequent fusion reactions. We examined the effects of genetic perturbation of α- and βSNAP expression on synaptic vesicle exocytosis, employing a new Ca2+ uncaging protocol to study synaptic vesicle trafficking, priming, and fusion in small glutamatergic synapses of hippocampal neurons. By characterizing this protocol, we show that synchronous and asynchronous transmitter release involve different Ca2+ sensors and are not caused by distinct releasable vesicle pools, and that tonic transmitter release is due to ongoing priming and fusion of new synaptic vesicles during high synaptic activity. Our analysis of α- and βSNAP deletion mutant neurons shows that the two NSF cofactors support synaptic vesicle priming by determining the availability of free SNARE components, particularly during phases of high synaptic activity.
| Original language | English |
|---|---|
| Pages (from-to) | 473-487 |
| Number of pages | 15 |
| Journal | Neuron |
| Volume | 68 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Nov 4 2010 |
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ASJC Scopus subject areas
- Neuroscience(all)
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SNARE Protein Recycling by αSNAP and βSNAP Supports Synaptic Vesicle Priming. / Burgalossi, Andrea; Jung, Sangyong; Meyer, Guido; Jockusch, Wolf J.; Jahn, Olaf; Taschenberger, Holger; O'Connor, Vincent M.; Nishiki, Tei-ichi; Takahashi, Masami; Brose, Nils; Rhee, Jeong Seop.
In: Neuron, Vol. 68, No. 3, 04.11.2010, p. 473-487.Research output: Contribution to journal › Article
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TY - JOUR
T1 - SNARE Protein Recycling by αSNAP and βSNAP Supports Synaptic Vesicle Priming
AU - Burgalossi, Andrea
AU - Jung, Sangyong
AU - Meyer, Guido
AU - Jockusch, Wolf J.
AU - Jahn, Olaf
AU - Taschenberger, Holger
AU - O'Connor, Vincent M.
AU - Nishiki, Tei-ichi
AU - Takahashi, Masami
AU - Brose, Nils
AU - Rhee, Jeong Seop
PY - 2010/11/4
Y1 - 2010/11/4
N2 - Neurotransmitter release proceeds by Ca2+-triggered, SNARE-complex-dependent synaptic vesicle fusion. After fusion, the ATPase NSF and its cofactors α- and βSNAP disassemble SNARE complexes, thereby recycling individual SNAREs for subsequent fusion reactions. We examined the effects of genetic perturbation of α- and βSNAP expression on synaptic vesicle exocytosis, employing a new Ca2+ uncaging protocol to study synaptic vesicle trafficking, priming, and fusion in small glutamatergic synapses of hippocampal neurons. By characterizing this protocol, we show that synchronous and asynchronous transmitter release involve different Ca2+ sensors and are not caused by distinct releasable vesicle pools, and that tonic transmitter release is due to ongoing priming and fusion of new synaptic vesicles during high synaptic activity. Our analysis of α- and βSNAP deletion mutant neurons shows that the two NSF cofactors support synaptic vesicle priming by determining the availability of free SNARE components, particularly during phases of high synaptic activity.
AB - Neurotransmitter release proceeds by Ca2+-triggered, SNARE-complex-dependent synaptic vesicle fusion. After fusion, the ATPase NSF and its cofactors α- and βSNAP disassemble SNARE complexes, thereby recycling individual SNAREs for subsequent fusion reactions. We examined the effects of genetic perturbation of α- and βSNAP expression on synaptic vesicle exocytosis, employing a new Ca2+ uncaging protocol to study synaptic vesicle trafficking, priming, and fusion in small glutamatergic synapses of hippocampal neurons. By characterizing this protocol, we show that synchronous and asynchronous transmitter release involve different Ca2+ sensors and are not caused by distinct releasable vesicle pools, and that tonic transmitter release is due to ongoing priming and fusion of new synaptic vesicles during high synaptic activity. Our analysis of α- and βSNAP deletion mutant neurons shows that the two NSF cofactors support synaptic vesicle priming by determining the availability of free SNARE components, particularly during phases of high synaptic activity.
UR - http://www.scopus.com/inward/record.url?scp=78049238166&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=78049238166&partnerID=8YFLogxK
U2 - 10.1016/j.neuron.2010.09.019
DO - 10.1016/j.neuron.2010.09.019
M3 - Article
C2 - 21040848
AN - SCOPUS:78049238166
VL - 68
SP - 473
EP - 487
JO - Neuron
JF - Neuron
SN - 0896-6273
IS - 3
ER -