Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 118, Issue 9, Pages -Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.2019194118
Keywords
amino-terminal domain; GluA1; LTP; AMPA; receptors; neuroplastin
Categories
Funding
- National Key R&D Program of China [2019YFA0801603, 2017YFA0105201]
- National Natural Science Foundation of China [91849112, 31571060, 31900698, 316708142, 81925011]
- Natural Science Foundation of Jiangsu Province [6E2019707]
- Beijing Municipal Commission of Science & Technology, and Education [Z181100001518001, CIT TCD20190334, KZ201910025025]
- Youth Beijing Scholars Program [015]
- Kay Realm R&D program of Guangdong Province [20196030335001]
- Fundamental Research Funds for the Central Universities [0903-14380029]
Ask authors/readers for more resources
Long-term potentiation (LTP) is a crucial cellular mechanism for learning and memory, with the amino-terminal domain (ATD) of GluA1 interacting with neuroplastin-65 (Np65) playing a key role in anchoring AMPARs at the postsynaptic membrane during LTP.
Long-term potentiation (LTP) has long been considered as an important cellular mechanism for learning and memory. LTP expression involves NMDA receptor-dependent synaptic insertion of AMPA receptors (AMPARs). However, how AMPARs are recruited and anchored at the postsynaptic membrane during LTP remains largely unknown. In this study, using CRISPR/Cas9 to delete the endogenous AMPARs and replace them with the mutant forms in single neurons, we have found that the amino-terminal domain (ATD) of GluA1 is required for LTP maintenance. Moreover, we show that GluA1 ATD directly interacts with the cell adhesion molecule neuroplastin-65 (Np65). Neurons lacking Np65 exhibit severely impaired LTP maintenance, and Np65 deletion prevents GluA1 from rescuing LTP in AMPARs-deleted neurons. Thus, our study reveals an essential role for GluA1/Np65 binding in anchoring AMPARs at the postsynaptic membrane during LTP.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available