NDLI: Ocular dominance plasticity is stably maintained in the absence of α calcium calmodulin kinase II (αCaMKII) autophosphorylation

Content Provider	PubMed Central
Author	Taha, Sharif A. Stryker, Michael P.
Copyright Year	2005
Abstract	The molecule α calcium calmodulin kinase II (αCaMKII) is known to play a fundamental role in the induction of many forms of synaptic plasticity. A major theory of αCaMKII function proposes that autophosphorylation of the molecule mediates not only the induction but also the maintenance of synaptic plasticity. To test this hypothesis, we assessed ocular dominance plasticity in genetically engineered mice that carry a mutation preventing autophosphorylation of αCaMKII. These mutant mice are deficient in plasticity after monocular deprivation, but a sufficiently long period of monocular deprivation will induce ocular dominance plasticity. After induction of ocular dominance plasticity, the stability of the induced changes was assayed after binocular deprivation. Plasticity in homozygous mutant animals was as stable as that measured in WT littermates; also, response characteristics did not differ between the two groups. Our results suggest that αCaMKII autophosphorylation is required for the induction of ocular dominance plasticity but is not needed for its stable maintenance thereafter.
Related Links	http://dx.doi.org/10.1073/pnas.0508185102
Ending Page	16442
Page Count	5
Starting Page	16438
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	45
Volume Number	102
Language	English
Publisher	National Academy of Sciences
Publisher Date	2005-11-08
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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