Angelo Marco, Plattner Florian, Giese K Peter
Wolfson Institute for Biomedical Research, University College London, London, UK.
J Neurochem. 2006 Oct;99(2):353-70. doi: 10.1111/j.1471-4159.2006.04040.x.
Cyclin-dependent kinase 5 (Cdk5) is a serine/threonine kinase with a multitude of functions. Although Cdk5 is widely expressed, it has been studied most extensively in neurons. Since its initial characterization, the fundamental contribution of Cdk5 to an impressive range of neuronal processes has become clear. These phenomena include neural development, dopaminergic function and neurodegeneration. Data from different fields have recently converged to provide evidence for the participation of Cdk5 in synaptic plasticity, learning and memory. In this review, we consider recent data implicating Cdk5 in molecular and cellular mechanisms underlying synaptic plasticity. We relate these findings to its emerging role in learning and memory. Particular attention is paid to the activation of Cdk5 by p25, which enhances hippocampal synaptic plasticity and memory, and suggests formation of p25 as a physiological process regulating synaptic plasticity and memory.
细胞周期蛋白依赖性激酶5（Cdk5）是一种具有多种功能的丝氨酸/苏氨酸激酶。尽管Cdk5广泛表达，但它在神经元中得到了最广泛的研究。自其最初被鉴定以来，Cdk5对一系列令人印象深刻的神经元过程的重要贡献已变得清晰。这些现象包括神经发育、多巴胺能功能和神经退行性变。来自不同领域的数据最近趋于一致，为Cdk5参与突触可塑性、学习和记忆提供了证据。在这篇综述中，我们考虑了最近表明Cdk5参与突触可塑性潜在分子和细胞机制的数据。我们将这些发现与其在学习和记忆中新兴的作用联系起来。特别关注p25对Cdk5的激活，它增强了海马体突触可塑性和记忆，并表明p25的形成是调节突触可塑性和记忆的生理过程。
