Wip1 phosphatase modulates both long-term potentiation and long-term depression through the dephosphorylation of CaMKII.
Cell Adh Migr
; 10(3): 237-47, 2016 05 03.
Article
em En
| MEDLINE
| ID: mdl-27158969
ABSTRACT
Synaptic plasticity is an important mechanism that underlies learning and cognition. Protein phosphorylation by kinases and dephosphorylation by phosphatases play critical roles in the activity-dependent alteration of synaptic plasticity. In this study, we report that Wip1, a protein phosphatase, is essential for long-term potentiation (LTP) and long-term depression (LTD) processes. Wip1-deletion suppresses LTP and enhances LTD in the hippocampus CA1 area. Wip1 deficiency-induced aberrant elevation of CaMKII T286/287 and T305 phosphorylation underlies these dysfunctions. Moreover, we showed that Wip1 modulates CaMKII dephosphorylation. Wip1(-/-) mice exhibit abnormal GluR1 membrane expression, which could be reversed by the application of a CaMKII inhibitor, indicating that Wip1/CaMKII signaling is crucial for synaptic plasticity. Together, our results demonstrate that Wip1 phosphatase plays a vital role in regulating hippocampal synaptic plasticity by modulating the phosphorylation of CaMKII.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Potenciação de Longa Duração
/
Depressão Sináptica de Longo Prazo
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Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina
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Proteína Fosfatase 2C
Limite:
Animals
Idioma:
En
Revista:
Cell Adh Migr
Ano de publicação:
2016
Tipo de documento:
Article
País de afiliação:
China