ArticleThe Journal of biological chemistry2010
Endogenous SNAP-25 regulates native voltage-gated calcium channels in glutamatergic neurons.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.
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Who cites it
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.
- Synaptic biomarkers in Alzheimer's disease dementia and mild cognitive impairment: A systematic review and meta-analysis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Pooled it
- The Association of SNAP25 Gene Polymorphisms in Attention Deficit/Hyperactivity Disorder: a Systematic Review and Meta-Analysis.Molecular neurobiology · 2017Pooled it
- Excitation-inhibition imbalance underlies perioperative neurocognitive disorders: a single-nucleus transcriptomic perspective in mice hippocampus.Molecular psychiatry · 2026Article
- Phenotypic diversity is caused by non-linear genetic interactions between two SNAREopathy genes.Molecular psychiatry · 2026Article
- Defining pain trajectories in juvenile arthritis and associated patient characteristics.Arthritis research & therapy · 2026Article
- Early and transient increase in cortical pyramidal cell excitability and delayed alteration of evoked synaptic transmission and t-SNARE proteins content in the hippocampus and neocortex of neonatal and juvenileFrontiers in cellular neuroscience · 2026Article
- Article
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- Minocycline Inhibits Tick-Borne Encephalitis Virus and Protects Infected Cells via Multiple Pathways.Viruses · 2024Article
- An updated review on animal models to study attention-deficit hyperactivity disorder.Translational psychiatry · 2024Review
- The Relationship between SNAP25 and Some Common Human Neurological Syndromes.Current pharmaceutical design · 2024Review
- Immune synaptopathies: how maternal immune activation impacts synaptic function during development.The EMBO journal · 2023Review
- Neuromuscular recovery from botulism involves multiple forms of compensatory plasticity.Frontiers in cellular neuroscience · 2023Article
- Mammalian Brain CaMembranes · 2022Article
- Invertebrate neurons as a simple model to study the hyperexcitable state of epileptic disorders in single cells, monosynaptic connections, and polysynaptic circuits.Biophysical reviews · 2022Review
- PRRT2 modulates presynaptic CaCell reports · 2021Article
- Exploring the Hereditary Nature of Migraine.Neuropsychiatric disease and treatment · 2021Review
- SNAP23 depletion enables more SNAP25/calcium channel excitosome formation to increase insulin exocytosis in type 2 diabetes.JCI insight · 2020Article
- Postsynaptic SNARE Proteins: Role in Synaptic Transmission and Plasticity.Neuroscience · 2019Review
- Interactions of Rabconnectin-3 with Cav2 calcium channels.Molecular brain · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to its primary role as a fundamental component of the SNARE complex, SNAP-25 also modulates voltage-gated calcium channels (VGCCs) in various overexpression systems. Although these studies suggest a potential negative regulatory role of SNAP-25 on VGCC activity, the effects of endogenous SNAP-25 on native VGCC function in neurons are unclear. In the present study, we investigated the VGCC properties of cultured glutamatergic and GABAergic rat hippocampal neurons. Glutamatergic currents were dominated by P/Q-type channels, whereas GABAergic cells had a dominant L-type component. Also, glutamatergic VGCC current densities were significantly lower with enhanced inactivation rates and shifts in the voltage dependence of activation and inactivation curves compared with GABAergic cells. Silencing endogenous SNAP-25 in glutamatergic neurons did not alter P/Q-type channel expression or localization but led to increased VGCC current density without changes in the VGCC subtype proportions. Isolation of the P/Q-type component indicated that increased current in the absence of SNAP-25 was correlated with a large depolarizing shift in the voltage dependence of inactivation. Overexpressing SNAP-25 in GABAergic neurons reduced current density without affecting the VGCC subtype proportion. Accordingly, VGCC current densities in glutamatergic neurons from Snap-25(+/-) mice were significantly elevated compared with wild type glutamatergic neurons. Overall, this study demonstrates that endogenous SNAP-25 negatively regulates native VGCCs in glutamatergic neurons which could have important implications for neurological diseases associated with altered SNAP-25 expression.
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