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[学习和记忆背后持久突触修饰的分子基础]

[Molecular basis of long-lasting synaptic modifications underlying learning and memory].

作者信息

Okuno Hiroyuki

机构信息

Medical Innovation Center, Kyoto University Graduate School of Medicine.

出版信息

Brain Nerve. 2013 Oct;65(10):1171-8.

Abstract

Neurons make contact with each other and form neuronal networks. The synapse, the site of contact between 2 neurons, has the ability to dynamically modify functional efficiency and connectivity in response to spatially and temporally specific patterns of neuronal activity. Such plastic ability of the synapse is believed to be indispensable for our cognitive functions, including learning and memory. In this review, I summarize our current understanding of the molecular and cellular mechanisms underlying synaptic plasticity. Lines of evidence have indicated that postsynaptic regulations of AMPA-type glutamate receptors (AMPA-Rs) are crucial for synaptic plasticity. Synaptic plasticity can be long-lasting if the local synaptic modifications interact with activity-dependent, newly synthesized plasticity-related molecules in the neuronal cell body. Recently, we found that the activity-regulated memory-related protein Arc is involved in synapse-specific regulation of AMPA-Rs. This Arc-dependent mechanism, together with other molecular mechanisms, possibly helps maintain the contrast of synaptic strength between strong and weak synapses, thus, promoting the formation of long-term memory.

摘要

神经元相互接触并形成神经网络。突触作为两个神经元之间的接触位点,能够根据神经元活动在空间和时间上的特定模式,动态地改变功能效率和连接性。突触的这种可塑性能力被认为是我们认知功能(包括学习和记忆)不可或缺的。在这篇综述中,我总结了我们目前对突触可塑性潜在分子和细胞机制的理解。有证据表明,AMPA型谷氨酸受体(AMPA-Rs)的突触后调节对突触可塑性至关重要。如果局部突触修饰与神经元细胞体中活动依赖的、新合成的可塑性相关分子相互作用,突触可塑性可能会持久。最近,我们发现活动调节的记忆相关蛋白Arc参与了AMPA-Rs的突触特异性调节。这种依赖Arc的机制,与其他分子机制一起,可能有助于维持强弱突触之间突触强度的差异,从而促进长期记忆的形成。

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