α-CaMKII-dependent plasticity in the cortex is required for permanent memory
α-CaMKII-dependent plasticity in the cortex is required for permanent memory
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DOI：
10.1038/35077089
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发表时间：
2001-05-17
期刊：
影响因子：
64.8
通讯作者：
Silva, AJ
中科院分区：
文献类型：
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作者：
Frankland, PW;O'Brien, C;Silva, AJ
皮质可塑性似乎对于永久记忆痕迹的建立至关重要(1-3)。然而，人们对于支持皮质网络记忆巩固的分子和细胞过程知之甚少(4,5)。在这里，我们发现，α-钙钙调蛋白激酶 II (α-CaMKII+/-) 零突变杂合小鼠在两项海马依赖性任务训练后 1-3 天表现出正常的学习和记忆能力。然而，如果保留时间较长（10-50 天），他们的记忆力就会受到严重损害。与此一致的是，我们发现α-CaMKII+/-小鼠的皮质长期增强作用受损，但海马体长期增强作用没有受损。我们的结果代表了揭示永久记忆建立的分子和细胞机制的第一步，它们表明α-CaMKII可能调节皮质网络中记忆痕迹巩固所需的突触事件。
Cortical plasticity seems to be critical for the establishment of permanent memory traces(1-3). Little is known, however, about the molecular and cellular processes that support consolidation of memories in cortical networks(4,5). Here we show that mice heterozygous for a null mutation of a-calcium-calmodulin kinase II (alpha -CaMKII+/-) show normal learning and memory 1-3 days after training in two hippocampus-dependent tasks. However, their memory is severely impaired at longer retention delays (10-50 days). Consistent with this, we found that alpha -CaMKII+/- mice have impaired cortical, but not hippocampal, long-term potentiation. Our results represent a first step in unveiling the molecular and cellular mechanisms underlying the establishment of permanent memories, and they indicate that alpha -CaMKII may modulate the synaptic events required for the consolidation of memory traces in cortical networks.