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Wip1 phosphatase modulates both long-term potentiation and long-term depression through the dephosphorylation of CaMKII.

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.

SUBMITTER: He ZY 

PROVIDER: S-EPMC4951180 | biostudies-literature | 2016 May

REPOSITORIES: biostudies-literature

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Wip1 phosphatase modulates both long-term potentiation and long-term depression through the dephosphorylation of CaMKII.

He Zhi-Yong ZY   Hu Wei-Yan WY   Zhang Ming M   Yang Zara Zhuyun ZZ   Zhu Hong-Mei HM   Xing Da D   Ma Quan-Hong QH   Xiao Zhi-Cheng ZC  

Cell adhesion & migration 20160509 3

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 elevat  ...[more]

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