Naskar, Souvik, Wan, Huimin and Kemenes, György (2014) pT305-CaMKII stabilizes a learning-induced increase in AMPA receptors for ongoing memory consolidation after classical conditioning. Nature Communications, 5. a3967. ISSN 2041-1723
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Abstract
The role of CaMKII in learning-induced activation and trafficking of AMPA receptors (AMPARs) is well established. However, the link between the phosphorylation state of CaMKII and the agonist-triggered proteasomal degradation of AMPARs during memory consolidation remains unknown. Here we describe a novel CaMKII-dependent mechanism by which a learning-induced increase in AMPAR levels is stabilized for consolidation of associative long-term memory. Six hours after classical conditioning the levels of both autophosphorylated pT305-CaMKII and GluA1 type AMPAR subunits are significantly elevated in the ganglia containing the learning circuits of the snail Lymnaea stagnalis. CaMKIINtide treatment significantly reduces the learning-induced elevation of both pT305-CaMKII and GluA1 levels and impairs associative long-term memory. Inhibition of proteasomal activity offsets the deleterious effects of CaMKIINtide on both GluA1 levels and long-term memory. These findings suggest that increased levels of pT305-CaMKII play a role in AMPAR-dependent memory consolidation by reducing proteasomal degradation of GluA1 receptor subunits.
Item Type: | Article |
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Schools and Departments: | School of Life Sciences > Neuroscience |
Research Centres and Groups: | Sussex Neuroscience |
Subjects: | Q Science > QP Physiology > QP0351 Neurophysiology and neuropsychology |
Depositing User: | George Kemenes |
Date Deposited: | 08 Sep 2014 10:14 |
Last Modified: | 28 Apr 2017 04:13 |
URI: | http://srodev.sussex.ac.uk/id/eprint/49707 |
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