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RETRACTED ARTICLE

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Elife. 2014 Aug 5;3:e03011. doi: 10.7554/eLife.03011.

Protein kinase C is a calcium sensor for presynaptic short-term plasticity.

Author information

1
Department of Neurobiology, Harvard Medical School, Boston, United States Center for Neuroscience, University of California, Davis, Davis, United States.
2
Department of Neurobiology, Harvard Medical School, Boston, United States.
3
The Biotechnology Center of Oslo, University of Oslo, Oslo, Norway.
4
Department of Neurobiology, Harvard Medical School, Boston, United States wade_regehr@hms.harvard.edu.

Abstract

In presynaptic boutons, calcium (Ca(2+)) triggers both neurotransmitter release and short-term synaptic plasticity. Whereas synaptotagmins are known to mediate vesicle fusion through binding of high local Ca(2+) to their C2 domains, the proteins that sense smaller global Ca(2+) increases to produce short-term plasticity have remained elusive. Here, we identify a Ca(2+) 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 Ca(2+)-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 Ca(2+) 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 Ca(2+) signals, and that Ca(2+) increases evoked by tetanic stimulation are sensed by PKCβ to produce PTP.DOI: http://dx.doi.org/10.7554/eLife.03011.001.

KEYWORDS:

calcium; phorbol ester; post-tetanic potentiation; protein kinase C; short-term plasticity; synaptotagmin

PMID:
25097249
PMCID:
PMC5841930
DOI:
10.7554/eLife.03011
[Indexed for MEDLINE]
Free PMC Article

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