ArticleNature neuroscience2013
Differential triggering of spontaneous glutamate release by P/Q-, N- and R-type Ca2+ channels.
Article in Nature neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
What it found
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Who cites it
91 citing papers in PubMed, 155 citations in OpenAlex.
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- High frequency stimulation activates hot spots of spontaneous synaptic transmission.Frontiers in synaptic neuroscience · 2025Article
- The intracellular C-terminus confers compartment-specific targeting of voltage-gated calcium channels.Cell reports · 2024Article
- Nano-organization of synaptic calcium signaling.Biochemical Society transactions · 2024Review
- Frequency of Spontaneous Neurotransmission at Individual Boutons Corresponds to the Size of the Readily Releasable Pool of Vesicles.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- The Mechanism of α2 adrenoreceptor-dependent Modulation of Neurotransmitter Release at the Neuromuscular Junctions.Neurochemical research · 2024Article
- Direct Current Stimulation Modulates Synaptic Facilitation via Distinct Presynaptic Calcium Channels.International journal of molecular sciences · 2023Article
- Spatially non-overlapping CaCell reports · 2023Article
- The release of inhibition model reproduces kinetics and plasticity of neurotransmitter release in central synapses.Communications biology · 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
- Cortical morphological heterogeneity of schizophrenia and its relationship with glutamatergic receptor variations.European psychiatry : the journal of the Association of European Psychiatrists · 2023Article
31 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 1 country.
Funding
Abstract
The role of voltage-gated Ca2+ channels (VGCCs) in spontaneous miniature neurotransmitter release is incompletely understood. We found that stochastic opening of P/Q-, N- and R-type VGCCs accounts for ∼50% of all spontaneous glutamate release at rat cultured hippocampal synapses, and that R-type channels have a far greater role in spontaneous than in action potential-evoked exocytosis. VGCC-dependent miniature neurotransmitter release (minis) showed similar sensitivity to presynaptic Ca2+ chelation as evoked release, arguing for direct triggering of spontaneous release by transient spatially localized Ca(2+) domains. Experimentally constrained three-dimensional diffusion modeling of Ca2+ influx-exocytosis coupling was consistent with clustered distribution of VGCCs in the active zone of small hippocampal synapses and revealed that spontaneous VGCCs openings can account for the experimentally observed VGCC-dependent minis, although single channel openings triggered release with low probability. Uncorrelated stochastic VGCC opening is therefore a major trigger for spontaneous glutamate release, with differential roles for distinct channel subtypes.
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