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首页> 外文期刊>Neuron >Knockout of ERK1 MAP Kinase Enhances Synaptic Plasticity in the Striatum and Facilitates Striatal-Mediated Learning and Memory.
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Knockout of ERK1 MAP Kinase Enhances Synaptic Plasticity in the Striatum and Facilitates Striatal-Mediated Learning and Memory.

机译:ERK1 MAP激酶的敲除可增强纹状体中的突触可塑性,并促进纹状体介导的学习和记忆。

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摘要

Extracellular signal-regulated kinases (ERK1 and 2) are synaptic signaling components necessary for several forms of learning. In mice lacking ERK1, we observe a dramatic enhancement of striatum-dependent long-term memory, which correlates with a facilitation of long-term potentiation in the nucleus accumbens. At the cellular level, we find that ablation of ERK1 results in a stimulus-dependent increase of ERK2 signaling, likely due to its enhanced interaction with the upstream kinase MEK. Consistently, such activity change is responsible for the hypersensitivity of ERK1 mutant mice to the rewarding properties of morphine. Our results reveal an unexpected complexity of ERK-dependent signaling in the brain and a critical regulatory role for ERK1 in the long-term adaptive changes underlying striatum-dependent behavioral plasticity and drug addiction.
机译:细胞外信号调节激酶(ERK1和2)是几种学习形式所必需的突触信号传导成分。在缺少ERK1的小鼠中,我们观察到纹状体依赖的长期记忆显着增强,这与伏隔核的长期增强作用有关。在细胞水平,我们发现ERK1的消融导致ERK2信号转导的刺激依赖性增加,可能是由于其与上游激酶MEK的相互作用增强。一致地,这种活性的变化是造成ERK1突变小鼠对吗啡的奖励特性过敏的原因。我们的研究结果揭示了大脑中ERK依赖性信号的意想不到的复杂性,以及ERK1在纹状体依赖性行为可塑性和药物成瘾的长期适应性变化中的关键调节作用。

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