ArticleScientific reports2017
Developmental stage-dependent regulation of spine formation by calcium-calmodulin-dependent protein kinase IIα and Rap1.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- CaMKII Drives Synaptic Maturation by Coordinating Spine Remodeling and Receptor Segregation via Liquid-Liquid Phase Separation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Epigenetic regulation ofFrontiers in psychiatry · 2025Article
- The dopamine analogue CA140 alleviates AD pathology, neuroinflammation, and rescues synaptic/cognitive functions by modulating DRD1 signaling or directly binding to Abeta.Journal of neuroinflammation · 2024Article
- The ISR downstream target ATF4 represses long-term memory in a cell type-specific manner.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Activity-Dependent Stabilization of Nascent Dendritic Spines Requires Nonenzymatic CaMKIIα Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Stress-mediated dysregulation of the Rap1 small GTPase impairs hippocampal structure and function.iScience · 2023Article
- Physics Clues on the Mind Substrate and Attributes.Frontiers in computational neuroscience · 2022Article
- Activity-regulated E3 ubiquitin ligase TRIM47 modulates excitatory synapse development.Frontiers in molecular neuroscience · 2022Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The roles of calcium-calmodulin-dependent protein kinase II-alpha (CaMKIIα) in the expression of long-term synaptic plasticity in the adult brain have been extensively studied. However, how increased CaMKIIα activity controls the maturation of neuronal circuits remains incompletely understood. Herein, we show that pyramidal neurons without CaMKIIα activity upregulate the rate of spine addition, resulting in elevated spine density. Genetic elimination of CaMKIIα activity specifically eliminated the observed maturation-dependent suppression of spine formation. Enhanced spine formation was associated with the stabilization of actin in the spine and could be reversed by increasing the activity of the small GTPase Rap1. CaMKIIα activity was critical in the phosphorylation of synaptic Ras GTPase-activating protein (synGAP), the dispersion of synGAP from postsynaptic sites, and the activation of postsynaptic Rap1. CaMKIIα is already known to be essential in learning and memory, but our findings suggest that CaMKIIα plays an important activity-dependent role in restricting spine density during postnatal development.
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