Calcium-dependent PKC isoforms have specialized roles in short-term synaptic plasticity.
Neuron
; 82(4): 859-71, 2014 May 21.
Article
em En
| MEDLINE
| ID: mdl-24794094
ABSTRACT
Posttetanic potentiation (PTP) is a widely observed form of short-term plasticity lasting for tens of seconds after high-frequency stimulation. Here we show that although protein kinase C (PKC) mediates PTP at the calyx of Held synapse in the auditory brainstem before and after hearing onset, PTP is produced primarily by an increased probability of release (p) before hearing onset, and by an increased readily releasable pool of vesicles (RRP) thereafter. We find that these mechanistic differences, which have distinct functional consequences, reflect unexpected differential actions of closely related calcium-dependent PKC isoforms. Prior to hearing onset, when PKCγ and PKCß are both present, PKCγ mediates PTP by increasing p and partially suppressing PKCß actions. After hearing onset, PKCγ is absent and PKCß produces PTP by increasing RRP. In hearing animals, virally expressed PKCγ overrides PKCß to produce PTP by increasing p. Thus, two similar PKC isoforms mediate PTP in distinctly different ways.
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Sinapses
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Proteína Quinase C
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Ponte
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Isoformas de Proteínas
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Neurônios
Idioma:
En
Ano de publicação:
2014
Tipo de documento:
Article