ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Kinase-dead knock-in mouse reveals an essential role of kinase activity of Ca2+/calmodulin-dependent protein kinase IIalpha in dendritic spine enlargement, long-term potentiation, and learning.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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83 citing papers in PubMed, 140 citations in OpenAlex.
- CaMKIIα mediates feedback effects of wheel-running activity on the circadian pacemaker in mice.Scientific reports · 2026Article
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- A Genome-wide Association Study of Alzheimer's Disease and Dementia in a Large Multi-ancestry Military Cohort Identifies Many New Dementia-Associated Loci.medRxiv : the preprint server for health sciences · 2026Article
- Multicolor Quantum Dot Tracking Uncovers Phenotypic Rescue of DAT A559V Aberrant Diffusion Upon D2R Antagonism.ACS chemical neuroscience · 2026Article
- The Janus face of CaMKII: from memory consolidation to neurotoxic switch in Alzheimer's disease.Archives of toxicology · 2025Review
- Effects of excessive iodine intake during the perinatal period on thyroid function and higher brain functions in mouse offspring.Endocrine journal · 2025Article
- A revised view of the role of CaMKII in learning and memory.Nature neuroscience · 2025Review
- Formation of long-term memory without short-term memory revealed by CaMKII inhibition.Nature neuroscience · 2025Article
- CaMKII autophosphorylation is the only enzymatic event required for synaptic memory.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Studying CaMKII: Tools and standards.Cell reports · 2024Review
- Activity-Dependent Stabilization of Nascent Dendritic Spines Requires Nonenzymatic CaMKIIα Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Synaptic memory and CaMKII.Physiological reviews · 2023Review
- Article
- A behavioral tagging account of kinase contribution to memory formation after spaced aversive training.iScience · 2023Article
- Role of Calcium Modulation in the Pathophysiology and Treatment of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Profiling the autoantibody repertoire reveals autoantibodies associated with mild cognitive impairment and dementia.Frontiers in neurology · 2023Article
- The Effects of Ninjinyoeito on Impaired Spatial Memory and Prefrontal Cortical Synaptic Plasticity throughEvidence-based complementary and alternative medicine : eCAM · 2023Article
- CaMKII: a central molecular organizer of synaptic plasticity, learning and memory.Nature reviews. Neuroscience · 2022Review
- Generation of Flag/DYKDDDDK Epitope Tag Knock-In Mice UsingInternational journal of molecular sciences · 2022Article
- Behind the scenes: Are latent memories supported by calcium independent plasticity?Hippocampus · 2022Review
23 more citing papers are in PubMed but not listed here.
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15 authors at 10 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca2+/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha) is an essential mediator of activity-dependent synaptic plasticity that possesses multiple protein functions. So far, the autophosphorylation site-mutant mice targeted at T286 and at T305/306 have demonstrated the importance of the autonomous activity and Ca2+/calmodulin-binding capacity of CaMKIIalpha, respectively, in the induction of long-term potentiation (LTP) and hippocampus-dependent learning. However, kinase activity of CaMKIIalpha, the most essential enzymatic function, has not been genetically dissected yet. Here, we generated a novel CaMKIIalpha knock-in mouse that completely lacks its kinase activity by introducing K42R mutation and examined the effects on hippocampal synaptic plasticity and behavioral learning. In homozygous CaMKIIalpha (K42R) mice, kinase activity was reduced to the same level as in CaMKIIalpha-null mice, whereas CaMKII protein expression was well preserved. Tetanic stimulation failed to induce not only LTP but also sustained dendritic spine enlargement, a structural basis for LTP, at the Schaffer collateral-CA1 synapse, whereas activity-dependent postsynaptic translocation of CaMKIIalpha was preserved. In addition, CaMKIIalpha (K42R) mice showed a severe impairment in inhibitory avoidance learning, a form of memory that is dependent on the hippocampus. These results demonstrate that kinase activity of CaMKIIalpha is a common critical gate controlling structural, functional, and behavioral expression of synaptic memory.
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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.