Protein kinase C is a calcium sensor for presynaptic short-term plasticity
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Fioravante, Diasynou
de Jong, Arthur PH
Leitges, Michael
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https://doi.org/10.7554/eLife.03011Metadata
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Fioravante, Diasynou, YunXiang Chu, Arthur PH de Jong, Michael Leitges, Pascal S Kaeser, and Wade G Regehr. 2014. “Protein kinase C is a calcium sensor for presynaptic short-term plasticity.” eLife 3 (1): e03011. doi:10.7554/eLife.03011. http://dx.doi.org/10.7554/eLife.03011.Abstract
In presynaptic boutons, calcium (Ca2+) triggers both neurotransmitter release and short-term synaptic plasticity. Whereas synaptotagmins are known to mediate vesicle fusion through binding of high local Ca2+ to their C2 domains, the proteins that sense smaller global Ca2+ increases to produce short-term plasticity have remained elusive. Here, we identify a Ca2+ sensor for post-tetanic potentiation (PTP), a form of plasticity thought to underlie short-term memory. We find that at the functionally mature calyx of Held synapse the Ca2+-dependent protein kinase C isoforms α and β are necessary for PTP, and the expression of PKCβ in PKCαβ double knockout mice rescues PTP. Disruption of Ca2+ binding to the PKCβ C2 domain specifically prevents PTP without impairing other PKCβ-dependent forms of synaptic enhancement. We conclude that different C2-domain-containing presynaptic proteins are engaged by different Ca2+ signals, and that Ca2+ increases evoked by tetanic stimulation are sensed by PKCβ to produce PTP. DOI: http://dx.doi.org/10.7554/eLife.03011.001Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121671/pdf/Terms of Use
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