Synaptic memory requires CaMKII

eLife

Joel Lee¹  Xiumin Chen¹  Javier Díaz-Alonso¹  Roger A Nicoll²  Jing Zhou³  Samuel Pleasure³  Wucheng Tao⁴ 

[1] Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, United States;Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, United States;Physiology, University of California, San Francisco, San Francisco, United States;Department of Neurology, University of California, San Francisco, San Francisco, United States;Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Medical University, Fuzhou, China;Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, United States;

关键词: synapse;    hippocampus;    LTP;    ion channel;    receptor;    camk2;    Mouse;   

DOI  :  10.7554/eLife.60360

来源: eLife Sciences Publications, Ltd

【 摘 要 】

Long-term potentiation (LTP) is arguably the most compelling cellular model for learning and memory. While the mechanisms underlying the induction of LTP (‘learning’) are well understood, the maintenance of LTP (‘memory’) has remained contentious over the last 20 years. Here, we find that Ca2+-calmodulin-dependent kinase II (CaMKII) contributes to synaptic transmission and is required LTP maintenance. Acute inhibition of CaMKII erases LTP and transient inhibition of CaMKII enhances subsequent LTP. These findings strongly support the role of CaMKII as a molecular storage device.

【 授权许可】

CC BY