Erasing sensorimotor memories via PKMzeta inhibition.

Erasing sensorimotor memories via PKMzeta inhibition.
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DOI:
10.1371/journal.pone.0011125
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发表时间:
2010-06-15
期刊:
影响因子:
3.7
通讯作者:
Francis JT
Francis JT
中科院分区:
综合性期刊3区
文献类型:
--
作者:
von Kraus LM;Sacktor TC;Francis JT

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感觉运动皮层在程序性学习中发挥作用。以前的研究表明,这种学习是由长时程增强(LTP),这反过来又维持了持续活跃的激酶,蛋白激酶Mzeta(PKM)。虽然PKM的作用,在动物模型中的陈述性知识的建立,其对程序性知识的影响还没有得到很好的理解。在这里,我们表明,PKM β抑制,通过注射zeta抑制肽(ZIP)到大鼠感觉运动皮层,破坏感觉运动记忆的熟练达到任务,即使经过几个星期的训练。在ZIP破坏记忆后重新学习任务的速度与初始学习的速度没有区别,这表明在记忆丧失后没有显著的节省。这些结果表明,陈述性和程序性记忆的储存有着共同的分子机制。
Sensorimotor cortex has a role in procedural learning. Previous studies suggested that this learning is subserved by long-term potentiation (LTP), which is in turn maintained by the persistently active kinase, protein kinase Mzeta (PKMζ). Whereas the role of PKMζ in animal models of declarative knowledge is established, its effect on procedural knowledge is not well understood. Here we show that PKMζ inhibition, via injection of zeta inhibitory peptide (ZIP) into the rat sensorimotor cortex, disrupts sensorimotor memories for a skilled reaching task even after several weeks of training. The rate of relearning the task after the memory disruption by ZIP was indistinguishable from the rate of initial learning, suggesting no significant savings after the memory loss. These results indicate a shared molecular mechanism of storage for declarative and procedural forms of memory.
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