ArticleProceedings of the National Academy of Sciences of the United States of America2009
Fos and Jun potentiate individual release sites and mobilize the reserve synaptic vesicle pool at the Drosophila larval motor synapse.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- MiR-92 Controls Synaptic Development Through Glial Vha55 Regulation.Biomolecules · 2025Article
- Presynaptic structural and functional plasticity are coupled by convergent Rap1 signaling.The Journal of cell biology · 2024Article
- scRNA-seq data from the larval Drosophila ventral cord provides a resource for studying motor systems function and development.Developmental cell · 2024Article
- Vav independently regulates synaptic growth and plasticity through distinct actin-based processes.The Journal of cell biology · 2022Article
- Systems Analysis of the 22q11.2 Microdeletion Syndrome Converges on a Mitochondrial Interactome Necessary for Synapse Function and Behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- The E3 ligase Highwire promotes synaptic transmission by targeting the NAD-synthesizing enzyme dNmnat.EMBO reports · 2019Article
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- Phosphorylation of Synaptojanin Differentially Regulates Endocytosis of Functionally Distinct Synaptic Vesicle Pools.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
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- Reactive Oxygen Species: Physiological and Physiopathological Effects on Synaptic Plasticity.Journal of experimental neuroscience · 2016Review
- Gene dosage in the dysbindin schizophrenia susceptibility network differentially affect synaptic function and plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Synaptic vesicle recycling: steps and principles.The EMBO journal · 2014Review
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- Behavioral and electrophysiological outcomes of tissue-specific Smn knockdown in Drosophila melanogaster.Brain research · 2012Article
- Differential control of presynaptic CaMKII activation and translocation to active zones.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Modeling spinal muscular atrophy in Drosophila links Smn to FGF signaling.The Journal of cell biology · 2011Article
- NFAT regulates pre-synaptic development and activity-dependent plasticity in Drosophila.Molecular and cellular neurosciences · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
In all nervous systems, short-term enhancement of transmitter release is achieved by increasing the weights of unitary synapses; in contrast, long-term enhancement, which requires nuclear gene expression, is generally thought to be mediated by the addition of new synaptic vesicle release sites. In Drosophila motor neurons, induction of AP-1, a heterodimer of Fos and Jun, induces cAMP- and CREB-dependent forms of presynaptic enhancement. Light and electron microscopic studies indicate that this synaptic enhancement is caused by increasing the weight of unitary synapses and not through the insertion of additional release sites. Electrophysiological and optical measurements of vesicle dynamics demonstrate that enhanced neurotransmitter release is accompanied by an increase in the actively cycling synaptic vesicle pool at the expense of the reserve pool. Finally, the observation that AP-1 mediated enhancement eliminates tetanus-induced forms of presynaptic potentiation suggests: (i) that reserve-pool mobilization is required for tetanus-induced short-term synaptic plasticity; and (ii) that long-term synaptic plasticity may, in some instances, be accomplished by stable recruitment of mechanisms that normally underlie short-term synaptic change.
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Registered trials
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