ArticleThe Journal of physiology1999
Depletion of calcium in the synaptic cleft of a calyx-type synapse in the rat brainstem.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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
63 citing papers in PubMed, 130 citations in OpenAlex.
- Mechanistic explanation of neuroplasticity using equivalent circuits.Frontiers in computational neuroscience · 2026Article
- Computational modeling predicts ephemeral acidic microdomains in the glutamatergic synaptic cleft.Biophysical journal · 2021Article
- Using ephaptic coupling to estimate the synaptic cleft resistivity of the calyx of Held synapse.PLoS computational biology · 2021Article
- Transmission at rod and cone ribbon synapses in the retina.Pflugers Archiv : European journal of physiology · 2021Review
- Interstitial ions: A key regulator of state-dependent neural activity?Progress in neurobiology · 2020Review
- Review
- CaProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Voltage- and calcium-gated ion channels of neurons in the vertebrate retina.Progress in retinal and eye research · 2019Review
- MCTP is an ER-resident calcium sensor that stabilizes synaptic transmission and homeostatic plasticity.eLife · 2017Article
- Dynamic Control of Synaptic Adhesion and Organizing Molecules in Synaptic Plasticity.Neural plasticity · 2017Review
- Glycolysis selectively shapes the presynaptic action potential waveform.Journal of neurophysiology · 2016Article
- Calcium-Sensing Receptor: A Key Target for Extracellular Calcium Signaling in Neurons.Frontiers in physiology · 2016Review
- Nanodomain coupling explains Ca²⁺ independence of transmitter release time course at a fast central synapse.eLife · 2014Article
- Article
- The Cav3-Kv4 complex acts as a calcium sensor to maintain inhibitory charge transfer during extracellular calcium fluctuations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- CALHM1 controls the Ca²⁺-dependent MEK, ERK, RSK and MSK signaling cascade in neurons.Journal of cell science · 2013Article
- Calcium, calpain, and calcineurin in low-frequency depression of transmitter release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Calcium homeostasis modulator 1 (CALHM1) is the pore-forming subunit of an ion channel that mediates extracellular Ca2+ regulation of neuronal excitability.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Modulation of T cell activation by localized K⁺ accumulation at the immunological synapse--a mathematical model.Journal of theoretical biology · 2012Article
- New insights into molecular players involved in neurotransmitter release.Physiology (Bethesda, Md.) · 2012Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. A new form of synaptic depression of excitatory synaptic transmission was observed when making voltage-clamp recordings from large presynaptic terminals, the calyces of Held and postsynaptic cells, the principal cells of the medial nucleus of the trapezoid body (MNTB), in slices of the rat auditory brainstem. 2. A short (100 ms) depolarization of the postsynaptic cell to 0 mV reduced the amplitude of the EPSCs by 35 +/- 5 % (n = 7), measured at 10 ms following the depolarization. Recovery occurred within 0.5 s. 3. The reduction of the EPSCs was most probably due to reduced presynaptic calcium influx, since postsynaptic depolarization reduced presynaptic calcium or barium currents. Conversely, presynaptic depolarization also reduced postsynaptic calcium or barium influx, under conditions where transmitter release was minimal. 4. The calcium currents and the postsynaptic depolarization-induced suppression of synaptic transmission recovered with a similar time course, suggesting that this form of synaptic depression was, most probably, due to depletion of Ca2+ in the synaptic cleft. 5. We conclude that when the Ca2+ influx into the pre- or postsynaptic cell is large, extracellular Ca2+ is depleted. Under these conditions, the Ca2+ concentration in the synaptic cleft is a sensitive indicator of the level of synaptic activity. However, the synaptic cleft is less sensitive to Ca2+ depletion than predicted from its estimated volume.
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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.