SSBD:database

Solveigh Cornelia Koeberle, Shinji Tanaka, Toshihiko Kuriu, Hirohide Iwasaki, Andreas Koeberle, Alexander Schulz, Dario-Lucas Helbing, Yoko Yamagata, Helen Morrison, Shigeo Okabe (2017) Developmental stage-dependent regulation of spine formation by calcium-calmodulin-dependent protein kinase IIalpha and Rap1., Scientific reports, Volume 7, Number 1, pp. 13409

Published in 2017 Oct 17 (Electronic publication in Oct. 17, 2017, midnight )

• doi: 10.1038/s41598-017-13728-y
• pmid: 29042611
  

(Abstract) The roles of calcium-calmodulin-dependent protein kinase II-alpha (CaMKIIalpha) in the expression of long-term synaptic plasticity in the adult brain have been extensively studied. However, how increased CaMKIIalpha activity controls the maturation of neuronal circuits remains incompletely understood. Herein, we show that pyramidal neurons without CaMKIIalpha activity upregulate the rate of spine addition, resulting in elevated spine density. Genetic elimination of CaMKIIalpha 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. CaMKIIalpha 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. CaMKIIalpha is already known to be essential in learning and memory, but our findings suggest that CaMKIIalpha plays an important activity-dependent role in restricting spine density during postnatal development.

• Animals
• Biomarkers
• Calcium/metabolism
• Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics[major]
• Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism
• Cell Differentiation/genetics[major]
• Dendritic Spines/metabolism[major]
• Fluorescent Antibody Technique
• Hippocampus
• Mice
• Models, Biological
• Neuronal Plasticity
• Neurons/cytology[major]
• Neurons/metabolism[major]
• Phosphorylation
• Protein Binding
• Pyramidal Cells/cytology
• Pyramidal Cells/metabolism
• rap1 GTP-Binding Proteins/genetics[major]
• rap1 GTP-Binding Proteins/metabolism