ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Protein kinase c increases the apparent affinity of the release machinery to Ca2+ by enhancing the release machinery downstream of the Ca2+ sensor.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 72 citations in OpenAlex.
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- Bidirectional modulation of glutamatergic synaptic transmission by metabotropic glutamate type 7 receptors at Schaffer collateral-CA1 hippocampal synapses.The Journal of physiology · 2018Article
- Single Bursts of Individual Granule Cells Functionally Rearrange Feedforward Inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Application of High-Throughput Assays to Examine Phospho-Modulation of the Late Steps of Regulated Exocytosis.High-throughput · 2017Article
- Regulation of insulin exocytosis by calcium-dependent protein kinase C in beta cells.Cell calcium · 2017Review
- Superpriming of synaptic vesicles as a common basis for intersynapse variability and modulation of synaptic strength.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Molecular mechanisms governing Ca(2+) regulation of evoked and spontaneous release.Nature neuroscience · 2015Review
- Calcium-dependent PKC isoforms have specialized roles in short-term synaptic plasticity.Neuron · 2014Article
- SynGAP regulates protein synthesis and homeostatic synaptic plasticity in developing cortical networks.PloS one · 2013Article
- Astroglial excitability and gliotransmission: an appraisal of Ca2+ as a signalling route.ASN neuro · 2012Review
- Calcium-dependent isoforms of protein kinase C mediate posttetanic potentiation at the calyx of Held.Neuron · 2011Article
- The metabotropic glutamate receptor mGlu7 activates phospholipase C, translocates munc-13-1 protein, and potentiates glutamate release at cerebrocortical nerve terminals.The Journal of biological chemistry · 2010Article
- Dynamic modulation of phasic and asynchronous glutamate release in hippocampal synapses.Journal of neurophysiology · 2010Article
- 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
- Action potential-independent and nicotinic receptor-mediated concerted release of multiple quanta at hippocampal CA3-mossy fiber synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Phosphorylation of SNAP-25 at Ser187 mediates enhancement of exocytosis by a phorbol ester in INS-1 cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Posttetanic potentiation critically depends on an enhanced Ca(2+) sensitivity of vesicle fusion mediated by presynaptic PKC.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Modulation of the release probability of releasable vesicles in response to Ca(2+) influx (Prob(Ca)) is involved in mediating several forms of synaptic plasticity, including short-term depression, short-term augmentation, and potentiation induced by protein kinases. Given such an important role, however, the mechanism underlying modulation of the Prob(Ca) is unclear. We addressed this question by investigating how the activation of protein kinase C modulates the Prob(Ca) at a calyx-type nerve terminal in rat brainstem. Various lengths of step depolarization were applied to the nerve terminal to evoke different amounts of Ca(2+) currents and capacitance jumps, the latter of which reflect vesicle release. The relationship between the capacitance jump and the Ca(2+) current integral was sigmoidal and was fit well with a Hill function. The sigmoidal relationship was shifted significantly to the left during the application of the PKC activator 12-myristate 13-acetate (PMA), suggesting that PMA increases the apparent affinity of the release machinery to Ca(2+). This effect was blocked in large part by the application of the PKC inhibitor bisindolylmaleimide, suggesting that the effect is mediated mainly by the activation of PKC. We also found that PMA increased the rate of miniature EPSCs evoked by the application of hypertonic sucrose solution, which triggers release downstream of the Ca(2+) influx. Taken together, our results suggest that PKC enhances the apparent affinity of the release machinery to Ca(2+) by a mechanism downstream of the binding between Ca(2+) and its sensor. These results have provided the first example of the mechanisms underlying modulation of the Prob(Ca).
Indexed as
Identifiers
11588166PMC6763846W2109578053What 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.