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CaMKII activation in the entorhinal cortex disrupts previously encoded spatial memory.

机译:内嗅皮层中的CaMKII激活破坏了先前编码的空间记忆。

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摘要

To investigate the role of the entorhinal cortex in memory at a molecular level, we developed transgenic mice in which transgene expression was inducible and limited to the superficial layers of the medial entorhinal cortex, pre- and parasubiculum. We found that expression of a constitutively active mutant form of CaMKII in these structures disrupted spatial memory formation. Immediate post-training activation of the transgene disrupted previously established memory while transgene activation 3 weeks following the training was ineffective. These results demonstrate that, similar to the hippocampus, the entorhinal cortex plays a time-limited role in spatial memory formation but is not a final cortical repository of long-term memory. Moreover, these results suggest that the indiscriminate activation of CaMKII is able to disrupt preexisting memories, possibly by altering the pattern of synaptic weight changes that are thought to form the basis of the memory trace.
机译:为了在分子水平上研究内嗅皮层在记忆中的作用,我们开发了转基因小鼠,其中转基因表达是可诱导的,并且仅限于内侧内嗅皮层,前和旁核的表层。我们发现在这些结构中CaMKII的组成型活性突变体形式的表达破坏了空间记忆的形成。训练后立即激活转基因会破坏先前建立的记忆,而训练后3周转基因激活无效。这些结果表明,与海马相似,内嗅皮层在空间记忆形成中发挥时间限制作用,但不是长期记忆的最终皮质储存库。而且,这些结果表明,CaMKII的不加选择的激活能够破坏先前存在的记忆,可能是通过改变被认为形成记忆痕迹基础的突触重量变化的模式来实现的。

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