ArticleProceedings of the National Academy of Sciences of the United States of America2012
Reduced release probability prevents vesicle depletion and transmission failure at dynamin mutant synapses.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 46 citations in OpenAlex.
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- Persistence of quantal synaptic vesicle recycling in virtual absence of dynamins.The Journal of physiology · 2025Article
- Effective knockdown-replace gene therapy in a novel mouse model of DNM1 developmental and epileptic encephalopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Evoked resonant neural activity long-term dynamics can be reproduced by a computational model with vesicle depletion.Neurobiology of disease · 2024Article
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- Reversal of cell, circuit and seizure phenotypes in a mouse model of DNM1 epileptic encephalopathy.Nature communications · 2023Article
- Synapse-Specific Defects in Synaptic Transmission in the Cerebellum of W246G Mutant ELOVL4 Rats-a Model of Human SCA34.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Accumbens D2-MSN hyperactivity drives antipsychotic-induced behavioral supersensitivity.Molecular psychiatry · 2021Article
- Dynamin deficiency causes insulin secretion failure and hyperglycemia.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Role of Calmodulin vs. Synaptotagmin in Exocytosis.Frontiers in molecular neuroscience · 2021Review
- Inositol Pyrophosphate Metabolism Regulates Presynaptic Vesicle Cycling at Central Synapses.iScience · 2020Article
- Neuronal BIN1 Regulates Presynaptic Neurotransmitter Release and Memory Consolidation.Cell reports · 2020Article
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- Prion acute synaptotoxicity is largely driven by protease-resistant PrPSc species.PLoS pathogens · 2018Article
- Article
- Molecular Mechanisms for the Coupling of Endocytosis to Exocytosis in Neurons.Frontiers in molecular neuroscience · 2017Review
- Dynamin-1 deletion enhances post-tetanic potentiation and quantal size after tetanic stimulation at the calyx of Held.The Journal of physiology · 2017Article
- Article
- Dynamin controls extracellular level of Awd/Nme1 metastasis suppressor protein.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Endocytic recycling of synaptic vesicles after exocytosis is critical for nervous system function. At synapses of cultured neurons that lack the two "neuronal" dynamins, dynamin 1 and 3, smaller excitatory postsynaptic currents are observed due to an impairment of the fission reaction of endocytosis that results in an accumulation of arrested clathrin-coated pits and a greatly reduced synaptic vesicle number. Surprisingly, despite a smaller readily releasable vesicle pool and fewer docked vesicles, a strong facilitation, which correlated with lower vesicle release probability, was observed upon action potential stimulation at such synapses. Furthermore, although network activity in mutant cultures was lower, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activity was unexpectedly increased, consistent with the previous report of an enhanced state of synapsin 1 phosphorylation at CaMKII-dependent sites in such neurons. These changes were partially reversed by overnight silencing of synaptic activity with tetrodotoxin, a treatment that allows progression of arrested endocytic pits to synaptic vesicles. Facilitation was also counteracted by CaMKII inhibition. These findings reveal a mechanism aimed at preventing synaptic transmission failure due to vesicle depletion when recycling vesicle traffic is backed up by a defect in dynamin-dependent endocytosis and provide new insight into the coupling between endocytosis and exocytosis.
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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.