Neuroscience Group, Division of Basic Biomedical Sciences, University of South Dakota, Sanford School of Medicine, Vermillion, SD 57069, USA.
Eur J Neurosci. 2010 Jul;32(2):269-77. doi: 10.1111/j.1460-9568.2010.07339.x. Epub 2010 Jul 14.
In the last few years it has become clear that AMPA-type glutamate neurotransmitter receptors are rapidly transported into and out of synapses to strengthen or weaken their function. The remarkable dynamics of AMPA receptor (AMPAR) synaptic localization provides a compelling mechanism for understanding the cellular basis of learning and memory, as well as disease states involving cognitive dysfunction. Here, we summarize the evidence for AMPAR trafficking as a mechanism underlying a variety of learned responses derived from both behavioral and cellular studies. Evidence is also reviewed supporting synaptic dysfunction related to impaired AMPAR trafficking as a mechanism underlying learning and memory deficits in Alzheimer's disease. We conclude that emerging data support the concept of multistage AMPAR trafficking during learning and that a broad approach to include examination of all of the AMPAR subunits will provide a more complete view of the mechanisms underlying multiple forms of learning.
在过去的几年中,人们已经清楚地认识到,AMPA 型谷氨酸神经递质受体可以快速在突触内运输,从而增强或减弱其功能。AMPA 受体 (AMPAR) 突触定位的显著动力学为理解学习和记忆的细胞基础以及涉及认知功能障碍的疾病状态提供了一个引人注目的机制。在这里,我们总结了 AMPAR 运输作为各种学习反应的基础机制的证据,这些反应来自行为和细胞研究。还回顾了支持与受损的 AMPAR 运输相关的突触功能障碍作为阿尔茨海默病学习和记忆缺陷的机制的证据。我们得出的结论是,新出现的数据支持在学习过程中 AMPAR 运输的多阶段概念,并且广泛的方法包括检查所有的 AMPAR 亚基将提供对多种形式学习的机制的更完整的认识。