ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 111 citations in OpenAlex.
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- Functional Nano-segregation of Distinct Forms of Neurotransmission.Advances in neurobiology · 2026Review
- Functionally distinct evoked and spontaneous neurotransmission operate via a shared pool of synaptic vesicles in viscerosensory afferents.The Journal of physiology · 2025Article
- The collapse of the wave function as the mediator of free will in prime neurons.Frontiers in neuroscience · 2025Article
- High frequency stimulation activates hot spots of spontaneous synaptic transmission.Frontiers in synaptic neuroscience · 2025Article
- Evaluation of mechanisms involved in regulation of intrinsic excitability by extracellular calcium in CA1 pyramidal neurons of rat.Journal of neurochemistry · 2025Article
- Calcium-sensing receptor regulates Kv7 channels via GBritish journal of pharmacology · 2024Article
- Pathological Interplay between Inflammation and Mitochondria Aggravates Glutamate Toxicity.International journal of molecular sciences · 2024Review
- Our Mental Health Is Determined by an Intrinsic Interplay between the Central Nervous System, Enteric Nerves, and Gut Microbiota.International journal of molecular sciences · 2023Review
- Spatially non-overlapping CaCell reports · 2023Article
- CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Axonal ER CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- L-type CaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Changes at glutamate tripartite synapses in the prefrontal cortex of a new animal model of resilience/vulnerability to acute stress.Translational psychiatry · 2023Article
- PLC regulates spontaneous glutamate release triggered by extracellular calcium and readily releasable pool size in neocortical neurons.Frontiers in cellular neuroscience · 2023Article
- Gut Bacteria and Neurotransmitters.Microorganisms · 2022Review
- Upregulated CaCells · 2022Article
- Synaptic Integration of Subquantal Neurotransmission by Colocalized G Protein-Coupled Receptors in Presynaptic Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Cinacalcet inhibition of neuronal action potentials preferentially targets the fast inactivated state of voltage-gated sodium channels.Frontiers in physiology · 2022Article
- Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Spontaneous release of glutamate is important for maintaining synaptic strength and controlling spike timing in the brain. Mechanisms regulating spontaneous exocytosis remain poorly understood. Extracellular calcium concentration ([Ca(2+)](o)) regulates Ca(2+) entry through voltage-activated calcium channels (VACCs) and consequently is a pivotal determinant of action potential-evoked vesicle fusion. Extracellular Ca(2+) also enhances spontaneous release, but via unknown mechanisms. Here we report that external Ca(2+) triggers spontaneous glutamate release more weakly than evoked release in mouse neocortical neurons. Blockade of VACCs has no effect on the spontaneous release rate or its dependence on [Ca(2+)](o). Intracellular [Ca(2+)] slowly increases in a minority of neurons following increases in [Ca(2+)](o). Furthermore, the enhancement of spontaneous release by extracellular calcium is insensitive to chelation of intracellular calcium by BAPTA. Activation of the calcium-sensing receptor (CaSR), a G-protein-coupled receptor present in nerve terminals, by several specific agonists increased spontaneous glutamate release. The frequency of spontaneous synaptic transmission was decreased in CaSR mutant neurons. The concentration-effect relationship for extracellular calcium regulation of spontaneous release was well described by a combination of CaSR-dependent and CaSR-independent mechanisms. Overall these results indicate that extracellular Ca(2+) does not trigger spontaneous glutamate release by simply increasing calcium influx but stimulates CaSR and thereby promotes resting spontaneous glutamate release.
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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.