ArticleProceedings of the National Academy of Sciences of the United States of America2006
Loss of AP-3 function affects spontaneous and evoked release at hippocampal mossy fiber synapses.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 57 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
57 citing papers in PubMed, 99 citations in OpenAlex.
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- Properties of Hippocampal Mossy Fibre Synapses in VAMP7 KO Mice.The European journal of neuroscience · 2025Article
- The release of inhibition model reproduces kinetics and plasticity of neurotransmitter release in central synapses.Communications biology · 2023Article
- Adaptor protein-3 produces synaptic vesicles that release phasic dopamine.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Adaptor protein AP-3 produces synaptic vesicles that release at high frequency by recruiting phospholipid flippase ATP8A1.Nature neuroscience · 2023Article
- A homozygous AP3D1 missense variant in patients with sensorineural hearing loss as the leading manifestation.Human genetics · 2023Article
- Synaptic Vesicle Recycling and the Endolysosomal System: A Reappraisal of Form and Function.Frontiers in synaptic neuroscience · 2022Review
- The function of VAMP2 in mediating membrane fusion: An overview.Frontiers in molecular neuroscience · 2022Review
- Single synapse glutamate imaging reveals multiple levels of release mode regulation in mammalian synapses.iScience · 2021Article
- Synaptic Vesicle Recycling Pathway Determines Neurotransmitter Content and Release Properties.Neuron · 2019Article
- Coordination of synaptic vesicle trafficking and turnover by the Rab35 signaling network.Small GTPases · 2019Review
- GPCR regulation of secretion.Pharmacology & therapeutics · 2018Review
- Postnatal Restriction of Activity-Induced CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Coupling of microtubule motors with AP-3 generated organelles in axons by NEEP21 family member calcyon.Molecular biology of the cell · 2018Article
- Comparative study of commercially available and homemade anti-VAMP7 antibodies using CRISPR/Cas9-depleted HeLa cells and VAMP7 knockout mice.F1000Research · 2018Article
- Loss of Doc2-Dependent Spontaneous Neurotransmission Augments Glutamatergic Synaptic Strength.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Selective molecular impairment of spontaneous neurotransmission modulates synaptic efficacy.Nature communications · 2017Article
- VGLUT2 Trafficking Is Differentially Regulated by Adaptor Proteins AP-1 and AP-3.Frontiers in cellular neuroscience · 2017Article
- Mechanisms, pools, and sites of spontaneous vesicle release at synapses of rod and cone photoreceptors.The European journal of neuroscience · 2016Article
- Functionally heterogeneous synaptic vesicle pools support diverse synaptic signalling.The Journal of physiology · 2016Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.