 |
|||||
|
|||||
|
|||||
|
|||||
|
|||||
The Journal of Neuroscience, November 19, 2003, 23(33):10645-10649
Previous Article | Next Article
Development/Plasticity/Repair
Calcium/Calmodulin-Dependent Protein Kinase II Contributes to Activity-Dependent Filopodia Growth and Spine Formation
Pascal Jourdain, Kohji Fukunaga,2 andDominique Muller1 1Neuropharmacology, University Medical Center, University of Geneva, 1211 Geneva 4, Switzerland, and 2Department of Pharmacology, Tohoku University Graduate School of Pharmaceutical Sciences, Sendai, Japan 980-8578
Remodeling of synaptic networks through an activity-dependent formation or elimination of synaptic connections is believed to contribute to information processing and long-term memory. Recent work showed that enhanced synaptic activation, including induction of long-term potentiation and sensory stimulation, promote a rapid growth of dendritic filopodia and the formation of new spines or new types of synapses. Here, we investigated whether calcium/calmodulin-dependent protein kinase II (CaMKII), an enzyme implicated in the control of synaptic efficacy, also participated in these mechanisms. We show that the intracellular application of autophosphorylated CaMKII reproduced these morphological changes and triggered filopodia growth and spine formation. In addition, we find that activation of endogenous kinase through the inhibition of phosphatases or the application of calmodulin in the cell produced similar effects. Conversely, blockade of CaMKII activity prevented the synaptic enhancement, the growth of filopodia and formation of new spines triggered by LTP induction, and a short anoxia/hypoglycemia. Together, these results support the interpretation that CaMKII contributes to the control of activity-dependent structural plasticity.
Key words: hippocampus; LTP (long-term potentiation); phosphorylation; synapse; synaptogenesis; confocal microscopy
Received July 8, 2003; revised September 17, 2003; accepted September 28, 2003.
This article has been cited by other articles:
L. Lo Iacono and C. Gross
{alpha}-Ca2+/Calmodulin-Dependent Protein Kinase II Contributes to the Developmental Programming of Anxiety in Serotonin Receptor 1A Knock-Out Mice
J. Neurosci., June 11, 2008; 28(24): 6250 - 6257.
[Abstract] [Full Text] [PDF]
S. V. Dindot, B. A. Antalffy, M. B. Bhattacharjee, and A. L. Beaudet
The Angelman syndrome ubiquitin ligase localizes to the synapse and nucleus, and maternal deficiency results in abnormal dendritic spine morphology
Hum. Mol. Genet., January 1, 2008; 17(1): 111 - 118.
[Abstract] [Full Text] [PDF]
M. De Roo, P. Klauser, P. Mendez, L. Poglia, and D. Muller
Activity-Dependent PSD Formation and Stabilization of Newly Formed Spines in Hippocampal Slice Cultures
Cereb Cortex, January 1, 2008; 18(1): 151 - 161.
[Abstract] [Full Text] [PDF]
B. Asrican, J. Lisman, and N. Otmakhov
Synaptic Strength of Individual Spines Correlates with Bound Ca2+ Calmodulin-Dependent Kinase II
J. Neurosci., December 19, 2007; 27(51): 14007 - 14011.
[Abstract] [Full Text] [PDF]
R. S. Vest, K. D. Davies, H. O'Leary, J. D. Port, and K. U. Bayer
Dual Mechanism of a Natural CaMKII Inhibitor
Mol. Biol. Cell, December 1, 2007; 18(12): 5024 - 5033.
[Abstract] [Full Text] [PDF]
U. V. Nagerl, G. Kostinger, J. C. Anderson, K. A. C. Martin, and T. Bonhoeffer
Protracted Synaptogenesis after Activity-Dependent Spinogenesis in Hippocampal Neurons
J. Neurosci., July 25, 2007; 27(30): 8149 - 8156.
[Abstract] [Full Text] [PDF]
G. M. Shankar, B. L. Bloodgood, M. Townsend, D. M. Walsh, D. J. Selkoe, and B. L. Sabatini
Natural Oligomers of the Alzheimer Amyloid-{beta} Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway
J. Neurosci., March 14, 2007; 27(11): 2866 - 2875.
[Abstract] [Full Text] [PDF]
S. L. Parsley, S. M. Pilgram, F. Soto, K. P. Giese, and F. A. Edwards
Enriching the environment of {alpha}CaMKIIT286A mutant mice reveals that LTD occurs in memory processing but must be subsequently reversed by LTP
Learn. Mem., January 1, 2007; 14(1-2): 75 - 83.
[Abstract] [Full Text] [PDF]
X.-m. Zha, J. A. Wemmie, S. H. Green, and M. J. Welsh
Acid-sensing ion channel 1a is a postsynaptic proton receptor that affects the density of dendritic spines
PNAS, October 31, 2006; 103(44): 16556 - 16561.
[Abstract] [Full Text] [PDF]
A. W. Grossman, G. M. Aldridge, I. J. Weiler, and W. T. Greenough
Local Protein Synthesis and Spine Morphogenesis: Fragile X Syndrome and Beyond
J. Neurosci., July 5, 2006; 26(27): 7151 - 7155.
[Abstract] [Full Text] [PDF]
Y. Shi and I. M. Ethell
Integrins Control Dendritic Spine Plasticity in Hippocampal Neurons through NMDA Receptor and Ca2+/Calmodulin-Dependent Protein Kinase II-Mediated Actin Reorganization
J. Neurosci., February 8, 2006; 26(6): 1813 - 1822.
[Abstract] [Full Text] [PDF]
A. J. Robison, M. A. Bass, Y. Jiao, L. B. MacMillan, L. C. Carmody, R. K. Bartlett, and R. J. Colbran
Multivalent Interactions of Calcium/Calmodulin-dependent Protein Kinase II with the Postsynaptic Density Proteins NR2B, Densin-180, and {alpha}-Actinin-2
J. Biol. Chem., October 21, 2005; 280(42): 35329 - 35336.
[Abstract] [Full Text] [PDF]
R. Andersen, Y. Li, M. Resseguie, and J. E. Brenman
Calcium/Calmodulin-Dependent Protein Kinase II Alters Structural Plasticity and Cytoskeletal Dynamics in Drosophila
J. Neurosci., September 28, 2005; 25(39): 8878 - 8888.
[Abstract] [Full Text] [PDF]
F. Tang and K. Kalil
Netrin-1 Induces Axon Branching in Developing Cortical Neurons by Frequency-Dependent Calcium Signaling Pathways
J. Neurosci., July 13, 2005; 25(28): 6702 - 6715.
[Abstract] [Full Text] [PDF]
R. T. Terry-Lorenzo, D. W. Roadcap, T. Otsuka, T. A. Blanpied, P. L. Zamorano, C. C. Garner, S. Shenolikar, and M. D. Ehlers
Neurabin/Protein Phosphatase-1 Complex Regulates Dendritic Spine Morphogenesis and Maturation
Mol. Biol. Cell, May 1, 2005; 16(5): 2349 - 2362.
[Abstract] [Full Text] [PDF]
|
|
|
|
 |
|