LTP研究在近十余年来一直是热点课题.尽管LTP是否是学习和记忆的基础仍有争议,肯定性的研究结果日趋增加,所以LTP仍吸引着大量研究工作者.近年来随着分子生物学技术的进步,人们得以借助转基因手段研究疾病相关性基因及其蛋白质,以及不明功能的基因和蛋白.转基因动物模型更是给难以模拟的Alzheimer氏病的研究极大推动.2001年人类基因组序列研究结果报告对医学科学的发展影响深远.应用转基因模型的手段进一步深入各研究领域.近几年来神经工作者借助转基因手段,对LTP的分子机制有了进一步认识.本文概括性介绍了这方面的有趣研究,希望读者能大致了解LTP研究进展,同时领悟转基因技术的推动力.%There is more and more evidence showing long term potentiation (LTP) is underling learning and memory even though it is still controversy and the mechanism behind LTP has not yet been completely understood. It is known that memory processes and long-term potentiation (LTP) are blocked at the time of their initiation by antagonists of glutamate NMDA or metabotropic receptors, and GABA-A receptor agonists. Following initiation, memory and LTP are accompanied by an enhancement of the activity of calcium/calmodulin-dependent protein kinase II and of protein kinase C. At the time of expression, LTP is blocked by antagonists of glutamate AMPA receptors. In recent five years, with advanced molecular biology techniques, scientist could use transgenic and knock out mice to explore what happens to LTP and learning and memory when specific disease related or novel gene was overexpressed or deleted. Therefore cellular and molecular mechanisms of activity-dependent synaptic plasticity are understood in a new level. Here we introduced recent research work on LTP with transgenic approach in hope to inspire interest in genomic and protenomic technology. We will continue to discuss BDNF and LTP and introduce some interesting LTP related work in part III.
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