Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Jan 18;12:413. doi: 10.1038/s41467-020-20523-3

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 8 — 1 Under baseline conditions synaptic transmission is mediated by GluA2-containing, calcium-impermeable (CI)-AMPARs, two shown for simplicity. 2 The first theta-burst stimulation (TBS) activates NMDA receptors (NMDARs) and this drives more CI-AMPARs into the synapse by lateral diffusion from a peri-synaptic pool, via a process that involves CaMKII. PKA is also activated (via adenyl cyclase, not shown) and this induces the process of inserting GluA2-lacking calcium-permeable (CP)-AMPARs into peri-synaptic sites on the plasma membrane. 3 LTP is expressed by the increase in number of CI-AMPARs (LTP_N) but synapses also become primed for LTP_γ by the availability of peri-synaptic CP-AMPARs. 4 Within ~1 h, the peri-synaptic CP-AMPARs are removed and, presumably, degraded. 6 If a second TBS is delivered whilst the synapses are still primed (5) then NMDAR activation drives the peri-synaptically located CP-AMPARs into the synapse, via a CaMKII-dependent process. This might involve an exchange of CP-AMPARs for CI-AMPARs, which are removed from the synapse via a mechanism triggered by PICK1. 7 These CP-AMPARs increase synaptic strength due to their higher single channel conductance (LTP_γ). However, their dwell time in the synapses is quite short (~15 min) before they are removed. If synapses remain active, such as by basal stimulation, activation of the transiently available, synaptic CP-AMPARs triggers protein synthesis and the insertion of more CI-AMPARs (8), which can extend the expression of LTP for long periods.