Autophosphorylation of αCaMKII is not a general requirement for NMDA receptor‐dependent LTP in the adult mouse
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Autophosphorylation of alpha-Ca2+/calmodulin kinase II (alphaCaMKII) at Thr286 is thought to be a general effector mechanism for sustaining transcription-independent long-term potentiation (LTP) at pathways where LTP is NMDA receptor-dependent. We have compared LTP at two such hippocampal pathways in mutant mice with a disabling point mutation at the Thr286 autophosphorylation site. We find that autophosphorylation of alphaCaMKII is essential for induction of LTP at Schaffer commissural-CA1 synapses in vivo, but is not required for LTP that can be sustained over days at medial perforant path-granule cell synapses in awake mice. At these latter synapses LTP is supported by cyclic AMP-dependent signalling in the absence of alphaCaMKII signalling. Thus, the autophosphorylation of alphaCaMKII is not a general requirement for NMDA receptor-dependent LTP in the adult mouse.
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NMDAR-dependent LTP is greatly impaired when T286 is replaced by T286A.
“Foremost are data, now long accepted, that NMDAR-dependent LTP is greatly impaired when T286 is replaced by T286A (43, 121, 381–384).”
From Synaptic memory and CaMKII (2023) · cites this paper as [383]
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- Authors
- Cooke, S. F., Wu, J., Plattner, F., Errington, M., Rowan, M., Peters, M., Hirano, A., Bradshaw, K. D., Anwyl, R., Bliss, T. V. P., & Giese, K. P.
- Affiliations
- Trinity College Dublin (IE)
- University College London (GB)
- National Institute for Medical Research (GB)
- Corresponding author
- Giese, K. Peter
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2006-07-21
- Volume
- 574
- Issue
- 3
- Pages
- 805-818
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC1817742
- OpenAlex
- W2166160073
- Cited by
- 77
- References
- 49
- Citations by year
- 2026: 3 · 2024: 2 · 2023: 2 · 2022: 5 · 2021: 3 · 2020: 4 · 2019: 2 · 2018: 3 · 2017: 1 · 2016: 2 · 2015: 8 · 2013: 3 · 2012: 4
- FWCI
- 3.28
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- Ernst Schering Foundation
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- CaMKIIα, autophosphorylation, long-term potentiation, NMDA receptor, hippocampus, cAMP signaling, synaptic plasticity, mouse mutants
- MeSH terms
- Action Potentials, Animals, Cells, Cultured, Hippocampus, Mice, Inbred C57BL, Phosphorylation, Signal Transduction, Receptors, N-Methyl-D-Aspartate, Mutagenesis, Site-Directed, Protein Serine-Threonine Kinases, Long-Term Potentiation, Amino Acid Substitution, Mice, Calcium-Calmodulin-Dependent Protein Kinase Kinase
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