ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Structural domains involved in the regulation of transmitter release by synapsins.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 141 citations in OpenAlex.
- An unsuspected physiological role for mGluRIII glutamate receptors in hippocampal area CA1.Cell reports · 2026Article
- Synapsin III promotes neuronal-like transdifferentiation of glioblastoma stem cells by disrupting JAG1-Notch1 interaction.Neuro-oncology · 2025Article
- Synapsin 2a tetramerisation selectively controls the presynaptic nanoscale organisation of reserve synaptic vesicles.Nature communications · 2024Article
- Synapsin condensation controls synaptic vesicle sequestering and dynamics.Nature communications · 2023Article
- Maternal synapsin autoantibodies are associated with neurodevelopmental delay.Frontiers in immunology · 2023Article
- Inhibition of Synaptic Glutamate Exocytosis and Prevention of Glutamate Neurotoxicity by Eupatilin fromInternational journal of molecular sciences · 2022Article
- Crosstalk of Synapsin1 palmitoylation and phosphorylation controls the dynamicity of synaptic vesicles in neurons.Cell death & disease · 2022Article
- An interaction between synapsin and C9orf72 regulates excitatory synapses and is impaired in ALS/FTD.Acta neuropathologica · 2022Article
- Synapsin II Directly Suppresses Epileptic Seizures In Vivo.Brain sciences · 2022Article
- Dyrk1a gene dosage in glutamatergic neurons has key effects in cognitive deficits observed in mouse models of MRD7 and Down syndrome.PLoS genetics · 2021Article
- Review
- How Postdoctoral Research in Paul Greengard's Laboratory Shaped My Scientific Career, Although I Never Did Another Phosphorylation Assay.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Article
- Correction of cognitive deficits in mouse models of Down syndrome by a pharmacological inhibitor of DYRK1A.Disease models & mechanisms · 2018Article
- Review
- Differential Expression of Synapsin I and II upon Treatment by Lithium and Valproic Acid in Various Brain Regions.The international journal of neuropsychopharmacology · 2018Article
- Molecular Mechanisms of Short-Term Plasticity: Role of Synapsin Phosphorylation in Augmentation and Potentiation of Spontaneous Glutamate Release.Frontiers in synaptic neuroscience · 2018Article
- Epitope specificity of anti-synapsin autoantibodies: Differential targeting of synapsin I domains.PloS one · 2018Article
- Immunoglobulin genotypes and cognitive functions in schizophrenia.Immunogenetics · 2018Article
- Calcium-Dependent and Synapsin-Dependent Pathways for the Presynaptic Actions of BDNF.Frontiers in cellular neuroscience · 2017Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Synapsins are a family of neuron-specific phosphoproteins that regulate neurotransmitter release by associating with synaptic vesicles. Synapsins consist of a series of conserved and variable structural domains of unknown function. We performed a systematic structure-function analysis of the various domains of synapsin by assessing the actions of synapsin fragments on neurotransmitter release, presynaptic ultrastructure, and the biochemical interactions of synapsin. Injecting a peptide derived from domain A into the squid giant presynaptic terminal inhibited neurotransmitter release in a phosphorylation-dependent manner. This peptide had no effect on vesicle pool size, synaptic depression, or transmitter release kinetics. In contrast, a peptide fragment from domain C reduced the number of synaptic vesicles in the periphery of the active zone and increased the rate and extent of synaptic depression. This peptide also slowed the kinetics of neurotransmitter release without affecting the number of docked vesicles. The domain C peptide, as well as another peptide from domain E that is known to have identical effects on vesicle pool size and release kinetics, both specifically interfered with the binding of synapsins to actin but not with the binding of synapsins to synaptic vesicles. This suggests that both peptides interfere with release by preventing interactions of synapsins with actin. Thus, interactions of domains C and E with the actin cytoskeleton may allow synapsins to perform two roles in regulating release, whereas domain A has an actin-independent function that regulates transmitter release in a phosphorylation-sensitive manner.
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Registered trials
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.