ArticleSynapse (New York, N.Y.)2020
CaMKII inhibitor 1 (CaMK2N1) mRNA is upregulated following LTP induction in hippocampal slices.
Article in Synapse (New York, N.Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
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- Human umbilical cord mesenchymal stem cell-derived exosomal miR-455-3p targets CAMK2N1 to improve trophoblast cell injury in gestational diabetes mellitus.Diabetology & metabolic syndrome · 2025Article
- A synapse-specific refractory period for plasticity at individual dendritic spines.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Microglia: The Drunken Gardeners of Early Adversity.Biomolecules · 2024Review
- A synapse-specific refractory period for plasticity at individual dendritic spines.bioRxiv : the preprint server for biology · 2024Article
- Transient Impairment in Microglial Function Causes Sex-Specific Deficits in Synaptic and Hippocampal Function in Mice Exposed to Early Adversity.bioRxiv : the preprint server for biology · 2024Article
- SGCAST: symmetric graph convolutional auto-encoder for scalable and accurate study of spatial transcriptomics.Briefings in bioinformatics · 2023Article
- DNA methylation signatures in human neonatal blood following maternal antenatal corticosteroid treatment.Translational psychiatry · 2022Article
- Heterogeneous CaMKII-Dependent Synaptic Compensations in CA1 Pyramidal Neurons From Acute Hippocampal Slices.Frontiers in cellular neuroscience · 2022Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
CaMK2N1 and CaMK2N2 (also known as CaMKIINα and β) are endogenous inhibitors of calcium/calmodulin-dependent kinase II (CaMKII), an enzyme critical for memory and long-term potentiation (LTP), a form of synaptic plasticity thought to underlie learning. CaMK2N1/2 mRNAs are rapidly and differentially upregulated in the hippocampus and amygdala after acquisition or retrieval of fear memory. Moreover, CaMK2N2 protein levels increase after contextual fear conditioning. Therefore, it was proposed that CaMK2N1/2 genes (Camk2n1/2) could be immediate-early genes transcribed promptly (30-60 min) after training. As a first approach to explore a role in synaptic plasticity, we assessed a possible regulation of Camk2n1/2 during the expression phase of LTP in hippocampal CA3-CA1 connections in rat brain slices. Quantitative PCR revealed that Camk2n1, but not Camk2n2, is upregulated 60 min after LTP induction by Schaffer collaterals high-frequency stimulation. We observed a graded, significant positive correlation between the magnitude of LTP and Camk2n1 change in individual slices, suggesting a coordinated regulation of these properties. If mRNA increment actually resulted in the protein upregulation in plasticity-relevant subcellular locations, CaMK2N1 may be involved in CaMKII fine-tuning during LTP maintenance or in the regulation of subsequent plasticity events (metaplasticity).
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