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http://purl.uniprot.org/citations/37993087http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/37993087http://www.w3.org/2000/01/rdf-schema#comment"

Objective

GluA1-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors (AMPARs) inserted into postsynaptic membranes are key to the process of long-term potentiation (LTP). Some evidence has shown that 4.1N plays a critical role in the membrane trafficking of AMPARs. However, the underlying mechanism behind this is still unclear. We investigated the role of 4.1N-mediated membrane trafficking of AMPARs during theta-burst stimulation long-term potentiation (TBS-LTP), to illustrate the molecular mechanism behind LTP.

Methods

LTP was induced by TBS in rat hippocampal CA1 neuron. Tat-GluA1 (MPR), which disrupts the association of 4.1N-GluA1, and autocamtide-2-inhibitory peptide, myristoylated (Myr-AIP), a CaMKII antagonist, were used to explore the role of 4.1N in the AMPARs trafficking during TBS-induced LTP. Immunoprecipitation (IP) and immunoblotting (IB)were used to detect protein expression, phosphorylation, and the interaction of p-CaMKII-4.1N-GluA1.

Results

We found that Myr-AIP attenuated increases of p-CaMKII (T286), p-GluA1 (ser831), and 4.1N phosphorylation after TBS-LTP, and decreased the association of p-CaMKII-4.1N-GluA1, along with the expression of GluA1, at postsynaptic densities during TBS-LTP. We also designed interfering peptides to disrupt the interaction between 4.1N and GluA1, which showed that Tat-GluA1 (MPR) or Myr-AIP inhibited TBS-LTP and attenuated increases of GluA1 at postsynaptic sites, while Tat-GluA1 (MPR) or Myr-AIP had no effects on miniature excitatory postsynaptic currents (mEPSCs) in non-stimulated hippocampal CA1 neurons.

Conclusion

Active CaMKII enhanced the phosphorylation of 4.1N and facilitated the association of p-CaMKII with 4.1N-GluA1, which in turn resulted in GluA1 trafficking during TBS-LTP. The association of 4.1N-GluA1 is required for LTP, but not for basal synaptic transmission."xsd:string
http://purl.uniprot.org/citations/37993087http://purl.org/dc/terms/identifier"doi:10.1016/j.neuroscience.2023.11.016"xsd:string
http://purl.uniprot.org/citations/37993087http://purl.uniprot.org/core/author"Liu Y."xsd:string
http://purl.uniprot.org/citations/37993087http://purl.uniprot.org/core/author"Yang J."xsd:string
http://purl.uniprot.org/citations/37993087http://purl.uniprot.org/core/author"Dong J.M."xsd:string
http://purl.uniprot.org/citations/37993087http://purl.uniprot.org/core/author"Hu S.Q."xsd:string
http://purl.uniprot.org/citations/37993087http://purl.uniprot.org/core/author"Yan J.Z."xsd:string
http://purl.uniprot.org/citations/37993087http://purl.uniprot.org/core/author"Ma R.N."xsd:string
http://purl.uniprot.org/citations/37993087http://purl.uniprot.org/core/date"2024"xsd:gYear
http://purl.uniprot.org/citations/37993087http://purl.uniprot.org/core/name"Neuroscience"xsd:string
http://purl.uniprot.org/citations/37993087http://purl.uniprot.org/core/pages"131-142"xsd:string
http://purl.uniprot.org/citations/37993087http://purl.uniprot.org/core/title"Phosphorylation of 4.1N by CaMKII Regulates the Trafficking of GluA1-containing AMPA Receptors During Long-term Potentiation in Acute Rat Hippocampal Brain Slices."xsd:string
http://purl.uniprot.org/citations/37993087http://purl.uniprot.org/core/volume"536"xsd:string
http://purl.uniprot.org/citations/37993087http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/37993087
http://purl.uniprot.org/citations/37993087http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/37993087
http://purl.uniprot.org/uniprot/#_A6HEN8-mappedCitation-37993087http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/37993087
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http://purl.uniprot.org/uniprot/#_P19490-mappedCitation-37993087http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/37993087
http://purl.uniprot.org/uniprot/#_Q924I5-mappedCitation-37993087http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/37993087
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http://purl.uniprot.org/uniprot/A6HEN9http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/37993087
http://purl.uniprot.org/uniprot/Q924I5http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/37993087
http://purl.uniprot.org/uniprot/A6HEN8http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/37993087
http://purl.uniprot.org/uniprot/P19490http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/37993087
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