ArticleThe Journal of physiology2000
Phosphorylation regulates spontaneous and evoked transmitter release at a giant terminal in the rat auditory brainstem.
Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Number and relative abundance of synaptic vesicles in functionally distinct priming states determine synaptic strength and short-term plasticity.The Journal of physiology · 2025Article
- Calcium-dependent isoforms of protein kinase C mediate posttetanic potentiation at the calyx of Held.Neuron · 2011Article
- Phorbol esters modulate spontaneous and Ca2+-evoked transmitter release via acting on both Munc13 and protein kinase C.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Differential control of two forms of glutamate release by group III metabotropic glutamate receptors at rat entorhinal synapses.Neuroscience · 2007Article
- Correlation of non-uniform protein expression with variation in transmitter release probability.Synapse (New York, N.Y.) · 2005Article
- Regulation of transmitter release by synapsin II in mouse motor terminals.The Journal of physiology · 2004Article
- Phorbol esters and adenosine affect the readily releasable neurotransmitter pool by different mechanisms at amphibian motor nerve endings.The Journal of physiology · 2003Article
- Phorbol esters and neurotransmitter release: more than just protein kinase C?British journal of pharmacology · 2003Review
- Specificity emerges in the dissection of diacylglycerol- and protein kinase C-mediated signalling pathways.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- A highly Ca2+-sensitive pool of vesicles is regulated by protein kinase C in adrenal chromaffin cells.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- A GDP/GTP exchange protein for the Rab3 small G protein family up-regulates a postdocking step of synaptic exocytosis in central synapses.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Increase in the pool size of releasable synaptic vesicles by the activation of protein kinase C in goldfish retinal bipolar cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Synaptic transmission in the auditory brainstem of normal and congenitally deaf mice.The Journal of physiology · 2002Article
- Ultrastructural basis of synaptic transmission between endbulbs of Held and bushy cells in the rat cochlear nucleus.The Journal of physiology · 2002Article
- Protein kinase c increases the apparent affinity of the release machinery to Ca2+ by enhancing the release machinery downstream of the Ca2+ sensor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Preferential potentiation of fast-releasing synaptic vesicles by cAMP at the calyx of Held.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
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. The role of phosphorylation in synaptic transmission was investigated at a large glutamatergic terminal, the endbulb of Held, on bushy cells in the rat anteroventral cochlear nucleus (AVCN). 2. Whole-cell recordings of excitatory postsynaptic currents (EPSCs) were used to examine the effects of kinase inhibitors and activators on low-frequency (baseline) evoked release, spontaneous release, paired-pulse facilitation (PPF) or depression (PPD), repetitive stimuli and recovery from depression. 3. Application of the kinase inhibitor H7 (100 microM) reduced low-frequency evoked EPSC amplitude (by 15 %) and simultaneously increased PPF (or reduced PPD), with no significant change in other aspects of transmission. H7 did not affect the amplitude or frequency of spontaneous miniature EPSCs. 4. Phorbol esters increased EPSC amplitude (by 50 %) with a concomitant decrease in PPF (or increase in PPD), and reduced the final EPSC amplitude during repetitive stimuli. The effect of phorbol esters was due exclusively to protein kinase C (PKC) activation, as the specific PKC inhibitor bis-indolylmaleimide (Bis) completely blocked the potentiating effect of phorbol esters on EPSC amplitude. 5. Significantly, phorbol esters did not increase the evoked EPSC amplitude at connections in which release was maximized using high extracellular calcium concentrations (4-6 mM). 6. Phorbol esters increased the frequency of spontaneous miniature EPSCs in physiological calcium (by 275 %), and in high extracellular calcium (by 210 %) when phorbol esters did not increase the evoked EPSC amplitude. 7. Our results are most consistent with the actions of H7 to decrease low-frequency release probability and phorbol esters to increase low-frequency release probability at the endbulb-bushy cell synaptic connection in the AVCN. The effects of H7 and phorbol esters on paired-pulse responses and tetanic depression appear to be largely consequential to these changes in low-frequency release probability.
Indexed as
Identifiers
What OpenQuestion holds
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.