ArticleNeuron2021
Role of Aberrant Spontaneous Neurotransmission in SNAP25-Associated Encephalopathies.
Article in Neuron, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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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Who cites it
48 citing papers in PubMed, 77 citations in OpenAlex.
- Lithium as a therapeutic strategy for SNAP25 encephalopathies via modulation of homeostatic plasticity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Dopaminergic tone inhibits spontaneous glutamate release and augments homeostatic synaptic plasticity.Molecular psychiatry · 2026Article
- SNAP-25 disease variants affect synaptic transmission by destabilizing SNARE complexes within a multimeric SNARE ring.Cell reports · 2026Article
- Regulation of spontaneous neurotransmission and homeostatic synaptic plasticity by synaptotagmin-1 disease variants at the SNARE primary interface.bioRxiv : the preprint server for biology · 2026Article
- Impact of distinct neurotransmitter release modes on neuronal signaling.Molecular psychiatry · 2026Review
- Baker-Gordon Syndrome-Associated Synaptotagmin-1 Mutations Reduce Synaptic Strength in Mouse Primary and Human-Induced Neuronal Culture Models.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Functional Nano-segregation of Distinct Forms of Neurotransmission.Advances in neurobiology · 2026Review
- Prognostic value of vascular endothelial growth factor subtypes and risk models constructed based on the common pathway of ulcerative colitis and colon cancer.Open medicine (Warsaw, Poland) · 2026Article
- Recent Structural Insights into the Molecular Architecture of Synapses.Advances in neurobiology · 2026Review
- Article
- Synaptobrevin-2 disease variants reveal spatial constraints within the presynaptic active zone.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Spontaneous glutamate release activates mGluR signaling to drive rapid antidepressant responses.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Bioinformatics-based identification of mirdametinib as a potential therapeutic target for idiopathic pulmonary fibrosis associated with endoplasmic reticulum stress.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Lysophosphatidic acid selectively modulates excitatory transmission in hippocampal neurons.Cell & bioscience · 2025Article
- The postsynaptic density in excitatory synapses is composed of clustered, heterogeneous nanoblocks.The Journal of cell biology · 2025Article
- SNAP25-dependent membrane trafficking of the Kv1.5 channel regulates the onset of atrial fibrillation.Nature communications · 2025Article
- Article
- Integrative mRNA and miRNA Expression Profiles from Developing Zebrafish Head Highlight Brain-Preference Genes and Regulatory Networks.Molecular neurobiology · 2025Article
- Repetitive Transcranial Magnetic Stimulation-Mediated Neuroprotection in the 5xFAD Mouse Model of Alzheimer's Disease Through GABRG2 and SNAP25 Modulation.Molecular neurobiology · 2025Article
- Epg5 links proteotoxic stress due to defective autophagic clearance and epileptogenesis inAutophagy · 2025Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
SNARE (soluble N-ethylmaleimide sensitive factor attachment protein receptor) complex, composed of synaptobrevin, syntaxin, and SNAP25, forms the essential fusion machinery for neurotransmitter release. Recent studies have reported several mutations in the gene encoding SNAP25 as a causative factor for developmental and epileptic encephalopathies of infancy and childhood with diverse clinical manifestations. However, it remains unclear how SNAP25 mutations give rise to these disorders. Here, we show that although structurally clustered mutations in SNAP25 give rise to related synaptic transmission phenotypes, specific alterations in spontaneous neurotransmitter release are a key factor to account for disease heterogeneity. Importantly, we identified a single mutation that augments spontaneous release without altering evoked release, suggesting that aberrant spontaneous release is sufficient to cause disease in humans.
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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.