ArticleNature communications2014
pT305-CaMKII stabilizes a learning-induced increase in AMPA receptors for ongoing memory consolidation after classical conditioning.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- A circuit mechanism linking past and future learning through shifts in perception.Science advances · 2023Article
- Role of densin-180 in mouse ventral hippocampal neurons in 24-hr retention of contextual fear conditioning.Brain and behavior · 2020Article
- Proactive and retroactive interference with associative memory consolidation in the snailCommunications biology · 2019Article
- Calcium/calmodulin-dependent kinase II and memory destabilization: a new role in memory maintenance.Journal of neurochemistry · 2018Review
- A CREB2-targeting microRNA is required for long-term memory after single-trial learning.Scientific reports · 2018Article
- Nitric Oxide Upregulates Proteasomal Protein Degradation in Neurons.Cellular and molecular neurobiology · 2017Article
- Structure-dependent effects of amyloid-β on long-term memory in Lymnaea stagnalis.FEBS letters · 2017Article
- CaMKII regulates proteasome phosphorylation and activity and promotes memory destabilization following retrieval.Neurobiology of learning and memory · 2016Article
- Opiate Exposure State Controls a D2-CaMKIIα-Dependent Memory Switch in the Amygdala-Prefrontal Cortical Circuit.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Postsynaptic insertion of AMPA receptor onto cortical pyramidal neurons in the anterior cingulate cortex after peripheral nerve injury.Molecular brain · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.