ArticlePloS one2014
Syntaxin 1B, but not syntaxin 1A, is necessary for the regulation of synaptic vesicle exocytosis and of the readily releasable pool at central synapses.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 86 citations in OpenAlex.
- STX1B variant-specific synaptic dysfunction is associated with network hyperexcitability in human iPSC-derived neurons.EBioMedicine · 2026Article
- Crotonylation of STXBP1 exacerbates seizure susceptibility by impairing GABAergic synaptic transmission.Cell death and differentiation · 2026Article
- Lipid Disorder and PIP2-Regulated Clustering of Syntaxin-1 JMD-TMD Regions Govern Membrane Fusion Competence.International journal of molecular sciences · 2026Article
- Transcriptomic Atlas of Human Trabecular Meshwork Uncovers the Cellular Landscape and Provides Insights into Glaucoma Pathophysiology.Research square · 2026Article
- A PIP2-stabilized syntaxin-1a structure mapped with transition metal ion FRET and unnatural fluorescent amino acids at the plasma membrane.Structure (London, England : 1993) · 2026Article
- Dual functions of SNAP25 in mouse taste buds.The Journal of physiology · 2025Article
- The sodium leak channel NALCN is regulated by neuronal SNARE complex proteins.Science advances · 2025Article
- Developmental and Epileptic Encephalopathy: Pathogenesis of Intellectual Disability Beyond Channelopathies.Biomolecules · 2025Review
- Messenger RNA transcription levels of neuronal soluble N-ethylmaleimide-sensitive factor attachment protein receptor complex components in the olfactory nerve system of the anadromous Pacific salmon, masu salmon Oncorhynchus masou.Fish physiology and biochemistry · 2024Article
- Repetitive pulsed-wave ultrasound stimulation suppresses neural activity by modulating ambient GABA levels via effects on astrocytes.Frontiers in cellular neuroscience · 2024Article
- Double mutation of open syntaxin and UNC-18 P334A leads to excitatory-inhibitory imbalance and impairs multiple aspects ofbioRxiv : the preprint server for biology · 2023Article
- The Molecular Mechanisms Employed by the ParasiteInternational journal of molecular sciences · 2023Article
- Syntabulin regulates neuronal excitation/inhibition balance and epileptic seizures by transporting syntaxin 1B.Cell death discovery · 2023Article
- Syntaxin-1 is necessary for UNC5A-C/Netrin-1-dependent macropinocytosis and chemorepulsion.Frontiers in molecular neuroscience · 2023Article
- Genetic disorders of neurotransmitter release machinery.Frontiers in synaptic neuroscience · 2023Review
- Vesicle trafficking with snares: a perspective for autism.Molecular biology reports · 2022Review
- The role of snare proteins in cortical development.Developmental neurobiology · 2022Review
- Knockdown of Piccolo in the Nucleus Accumbens Suppresses Methamphetamine-Induced Hyperlocomotion and Conditioned Place Preference in Mice.Neurochemical research · 2022Article
- Differential impairment of cerebrospinal fluid synaptic biomarkers in the genetic forms of frontotemporal dementia.Alzheimer's research & therapy · 2022Article
- Synaptopathies in Developmental and Epileptic Encephalopathies: A Focus on Pre-synaptic Dysfunction.Frontiers in neurology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two syntaxin 1 (STX1) isoforms, HPC-1/STX1A and STX1B, are coexpressed in neurons and function as neuronal target membrane (t)-SNAREs. However, little is known about their functional differences in synaptic transmission. STX1A null mutant mice develop normally and do not show abnormalities in fast synaptic transmission, but monoaminergic transmissions are impaired. In the present study, we found that STX1B null mutant mice died within 2 weeks of birth. To examine functional differences between STX1A and 1B, we analyzed the presynaptic properties of glutamatergic and GABAergic synapses in STX1B null mutant and STX1A/1B double null mutant mice. We found that the frequency of spontaneous quantal release was lower and the paired-pulse ratio of evoked postsynaptic currents was significantly greater in glutamatergic and GABAergic synapses of STX1B null neurons. Deletion of STX1B also accelerated synaptic vesicle turnover in glutamatergic synapses and decreased the size of the readily releasable pool in glutamatergic and GABAergic synapses. Moreover, STX1A/1B double null neurons showed reduced and asynchronous evoked synaptic vesicle release in glutamatergic and GABAergic synapses. Our results suggest that although STX1A and 1B share a basic function as neuronal t-SNAREs, STX1B but not STX1A is necessary for the regulation of spontaneous and evoked synaptic vesicle exocytosis in fast transmission.
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