期刊
ELIFE
卷 3, 期 -, 页码 -出版社
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.03011
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资金
- National Institute of Neurological Disorders and Stroke [R01NS032405, T32NS007484]
- National Institute on Drug Abuse [K01DA029044]
- National Institute on Deafness and Other Communication Disorders [F30-DC013716-01]
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek [NWO 825.12.028]
- Howard Hughes Medical Institute
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 alpha and beta are necessary for PTP, and the expression of PKC beta in PKC alpha beta double knockout mice rescues PTP. Disruption of Ca2+ binding to the PKC beta C2 domain specifically prevents PTP without impairing other PKC beta-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 PKC beta to produce PTP.
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