Kinase activity is not required for alphaCaMKII-dependent presynaptic plasticity at CA3-CA1 synapses.
Nat Neurosci
; 10(9): 1125-7, 2007 Sep.
Article
em En
| MEDLINE
| ID: mdl-17660813
ABSTRACT
Using targeted mouse mutants and pharmacologic inhibition of alphaCaMKII, we demonstrate that the alphaCaMKII protein, but not its activation, autophosphorylation or its ability to phosphorylate synapsin I, is required for normal short-term presynaptic plasticity. Furthermore, alphaCaMKII regulates the number of docked vesicles independent of its ability to be activated. These results indicate that alphaCaMKII has a nonenzymatic role in short-term presynaptic plasticity at hippocampal CA3-CA1 synapses.
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Base de dados:
MEDLINE
Assunto principal:
Sinapses
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Terminações Pré-Sinápticas
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Transmissão Sináptica
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Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina
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Hipocampo
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Plasticidade Neuronal
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Neurônios
Limite:
Animals
Idioma:
En
Ano de publicação:
2007
Tipo de documento:
Article