Elevated RalA activity in the hippocampus of PI3K gamma knock-out mice lacking NMDAR-dependent long-term depression

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Phosphoinositide 3-kinases (PI3Ks) play key roles in synaptic plasticity and cognitive functions in the brain. We recently found that genetic deletion of PI3K gamma, the only known member of class IB PI3Ks, results in impaired N-methyl-D-aspartate receptor-dependent long-term depression (NMDAR-LTD) in the hippocampus. The activity of RalA, a small GTP-binding protein, increases following NMDAR-LTD inducing stimuli, and this increase in RalA activity is essential for inducing NMDAR-LTD. We found that RalA activity increased significantly in PI3K gamma knockout mice. Furthermore, NMDAR-LTD-inducing stimuli did not increase RalA activity in PI3K gamma knockout mice. These results suggest that constitutively increased RalA activity occludes further increases in RalA activity during induction of LTD, causing impaired NMDAR-LTD. We propose that PI3K gamma regulates the activity of RalA, which is one of the molecular mechanisms inducing NMDAR-dependent LTD. [BMB Reports 2013; 46(2): 103-106]
Publisher
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
Issue Date
2013-02
Language
English
Article Type
Article
Keywords

PHOSPHATIDYLINOSITOL 3-KINASE; ACTIVATION; CELLS; POTENTIATION; TRAFFICKING; INHIBITION; MECHANISMS; EXPRESSION; PLASTICITY; INDUCTION

Citation

BMB REPORTS, v.46, no.2, pp.103 - 106

ISSN
1976-6696
DOI
10.5483/BMBRep.2013.46.2.143
URI
http://hdl.handle.net/10203/174870
Appears in Collection
BS-Journal Papers(저널논문)
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