Protein kinase C is a calcium sensor for presynaptic short-term plasticity.
Elife
; 3: e03011, 2014 Aug 05.
Article
en En
| MEDLINE
| ID: mdl-25097249
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 ß are necessary for PTP, and the expression of PKCß in PKCαß double knockout mice rescues PTP. Disruption of Ca(2+) binding to the PKCß C2 domain specifically prevents PTP without impairing other PKCß-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 PKCß to produce PTP.DOI http//dx.doi.org/10.7554/eLife.03011.001.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Señalización del Calcio
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Proteína Quinasa C-alfa
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Proteína Quinasa C beta
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Plasticidad Neuronal
Límite:
Animals
Idioma:
En
Revista:
Elife
Año:
2014
Tipo del documento:
Article
País de afiliación:
Estados Unidos