Synaptic memory requires CaMKII-Reference-Cited by-同舟云学术

Synaptic memory requires CaMKII

Published:2021-12-15 Issue: Volume:10 Page:
ISSN:2050-084X
Container-title:eLife
language:en
Short-container-title:

Author:

Tao Wucheng¹²^ORCID,Lee Joel²,Chen Xiumin²,Díaz-Alonso Javier²^ORCID,Zhou Jing³^ORCID,Pleasure Samuel³^ORCID,Nicoll Roger A²⁴^ORCID

Affiliation:

1. Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Medical University

2. Department of Cellular and Molecular Pharmacology, University of California, San Francisco

3. Department of Neurology, University of California, San Francisco

4. Physiology, University of California, San Francisco

Abstract

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.

Funder

National Institutes of Health

Publisher

eLife Sciences Publications, Ltd

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

Link

https://cdn.elifesciences.org/articles/60360/elife-60360-v2.pdf

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