The role of α-CaMKII autophosphorylation in neocortical experience-dependent plasticity
The role of α-CaMKII autophosphorylation in neocortical experience-dependent plasticity
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DOI：
10.1038/78820
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发表时间：
2000-09-01
影响因子：
25
通讯作者：
Fox, K
中科院分区：
文献类型：
--
作者：
Glazewski, S;Giese, KP;Fox, K
钙/钙调蛋白激酶II型（CaMKII）是一种主要的突触后密度蛋白。CaMKII被认为是一个“分子开关”，当被钙流入的短暂上升触发时，由于其自磷酸化的能力，它会长时间活跃。我们研究了携带α -CaMKII基因（T286A）点突变的小鼠桶状皮质的经验依赖性可塑性，该突变会消除该酶的自磷酸化能力。突变纯合子的成年和青春期小鼠的可塑性被阻止，但在杂合子和野生型幼崽中是正常的。这些结果证明了分子开关假说对新皮层经验依赖的可塑性是有效的。
Calcium/calmodulin kinase type II (CaMKII) is a major postsynaptic density protein. CaMKII is postulated to act as a 'molecular switch', which, when triggered by a transient rise in calcium influx, becomes active for prolonged periods because of its ability to autophosphorylate. We studied experience-dependent plasticity in the barrel cortex of mice carrying a point mutation of the alpha -CaMKII gene (T286A), which abolishes this enzyme's ability to autophosphorylate. Plasticity was prevented in adult and adolescent mice homozygous for the mutation, but was normal in heterozygotes and wild-type littermates. These results provide evidence that the molecular switch hypothesis is valid for neocortical experience-dependent plasticity.