Inhibitory autophosphorylation of CaMKII controls PSD association, plasticity, and learning

被引：237

作者：

Elgersma, Y

Fedorov, NB

Ikonen, S

Choi, ES

Elgersma, M

Carvalho, OM

Giese, KP

Silva, AJ ^{[1
]}

机构：

[1] Univ Calif Los Angeles, Dept Neurobiol, Los Angeles, CA 90095 USA

[2] Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA 90095 USA

[3] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA

[4] Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90095 USA

[5] Erasmus MC, Dept Neurosci, NL-3000 DR Rotterdam, Netherlands

来源：

NEURON | 2002年 / 36卷 / 03期

关键词：

D O I：

10.1016/S0896-6273(02)01007-3

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

To investigate the function of the a calcium-calmodulin-dependent kinase II (alphaCaMKII) inhibitory autophosphorylation at threonines 305 and/or 306, we generated knockin mice that express alphaCaMKII that cannot undergo inhibitory phosphorylation. In addition, we generated mice that express the inhibited form of alphaCaMKII, which resembles the persistently phosphorylated kinase at these sites. Our data demonstrate that blocking inhibitory phosphorylation increases CaMKII in the postsynaptic density (PSD), lowers the threshold for hippocampal long-term potentiation (LTP), and results in hippocampal-dependent learning that seems more rigid and less fine-tuned. Mimicking inhibitory phosphorylation dramatically decreased the association of CaMKII with the PSD and blocked both LTP and learning. These data demonstrate that inhibitory phosphorylation has a critical role in plasticity and learning.

引用

页码：493 / 505

页数：13

共 43 条

[1] Computer-assisted behavioral assessment of pavlovian fear conditioning in mice [J].