dorsal/arxiv
View SchemaLoss of AP-3 function affects spontaneous and evoked release at hippocampal mossy fiber synapses
| Authors | Anita Scheuber, Rachel Rudge, Lydia Danglot, Graca Raposo, Thomas Binz, Jean-Christophe Poncer, Thierry Galli |
|---|---|
| Categories | |
| ArXiv ID | q-bio/0610056 |
| URL | https://arxiv.org/abs/q-bio/0610056 |
| DOI | 10.1073/pnas.0603511103 |
| Journal | Proc Natl Acad Sci U S A (20/10/2006) sous presse |
Abstract
Synaptic vesicle (SV) exocytosis mediating neurotransmitter release occurs spontaneously at low intraterminal calcium concentrations and is stimulated by a rise in intracellular calcium. Exocytosis is compensated for by the reformation of vesicles at plasma membrane and endosomes. Although the adaptor complex AP-3 was proposed to be involved in the formation of SVs from endosomes, whether its function has an indirect effect on exocytosis remains unknown. Using mocha mice, which are deficient in functional AP-3, we identify an AP-3-dependent tetanus neurotoxin-resistant asynchronous release that can be evoked at hippocampal mossy fiber (MF) synapses. Presynaptic targeting of the tetanus neurotoxin-resistant vesicle soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) tetanus neurotoxin-insensitive vesicle-associated membrane protein (TI-VAMP) is lost in mocha hippocampal MF terminals, whereas the localization of synaptobrevin 2 is unaffected. In addition, quantal release in mocha cultures is more frequent and more sensitive to sucrose. We conclude that lack of AP-3 results in more constitutive secretion and loss of an asynchronous evoked release component, suggesting an important function of AP-3 in regulating SV exocytosis at MF terminals.
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"abstract": "Synaptic vesicle (SV) exocytosis mediating neurotransmitter release occurs\nspontaneously at low intraterminal calcium concentrations and is stimulated by\na rise in intracellular calcium. Exocytosis is compensated for by the\nreformation of vesicles at plasma membrane and endosomes. Although the adaptor\ncomplex AP-3 was proposed to be involved in the formation of SVs from\nendosomes, whether its function has an indirect effect on exocytosis remains\nunknown. Using mocha mice, which are deficient in functional AP-3, we identify\nan AP-3-dependent tetanus neurotoxin-resistant asynchronous release that can be\nevoked at hippocampal mossy fiber (MF) synapses. Presynaptic targeting of the\ntetanus neurotoxin-resistant vesicle soluble N-ethylmaleimide-sensitive factor\nattachment protein receptor (SNARE) tetanus neurotoxin-insensitive\nvesicle-associated membrane protein (TI-VAMP) is lost in mocha hippocampal MF\nterminals, whereas the localization of synaptobrevin 2 is unaffected. In\naddition, quantal release in mocha cultures is more frequent and more sensitive\nto sucrose. We conclude that lack of AP-3 results in more constitutive\nsecretion and loss of an asynchronous evoked release component, suggesting an\nimportant function of AP-3 in regulating SV exocytosis at MF terminals.",
"arxiv_id": "q-bio/0610056",
"authors": [
"Anita Scheuber",
"Rachel Rudge",
"Lydia Danglot",
"Graca Raposo",
"Thomas Binz",
"Jean-Christophe Poncer",
"Thierry Galli"
],
"categories": [
"q-bio.NC",
"q-bio.SC"
],
"doi": "10.1073/pnas.0603511103",
"journal_ref": "Proc Natl Acad Sci U S A (20/10/2006) sous presse",
"title": "Loss of AP-3 function affects spontaneous and evoked release at hippocampal mossy fiber synapses",
"url": "https://arxiv.org/abs/q-bio/0610056"
},
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