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dc.contributor.authorOtmakhov, Nikolai  Concept link
dc.contributor.authorTao-Cheng, Jung-Hwa  Concept link
dc.contributor.authorCarpenter, Stephen  Concept link
dc.contributor.authorAsrican, Brent  Concept link
dc.contributor.authorDosemeci, Ayse  Concept link
dc.contributor.authorReese, Thomas S.  Concept link
dc.contributor.authorLisman, John E.  Concept link
dc.date.accessioned2009-08-25T18:51:42Z
dc.date.available2009-08-25T18:51:42Z
dc.date.issued2004-10-20
dc.identifier.citationJournal of Neuroscience 24 (2004): 9324-9331en
dc.identifier.urihttps://hdl.handle.net/1912/2961
dc.descriptionAuthor Posting. © Society for Neuroscience, 2004. This article is posted here by permission of Society for Neuroscience for personal use, not for redistribution. The definitive version was published in Journal of Neuroscience 24 (2004): 9324-9331, doi:10.1523/JNEUROSCI.2350-04.2004.en
dc.description.abstractCalcium/calmodulin-dependent protein kinase II (CaMKII) is a leading candidate for a synaptic memory molecule because it is persistently activated after long-term potentiation (LTP) induction and because mutations that block this persistent activity prevent LTP and learning. Previous work showed that synaptic stimulation causes a rapidly reversible translocation of CaMKII to the synaptic region. We have now measured green fluorescent protein (GFP)-CaMKIIα translocation into synaptic spines during NMDA receptor-dependent chemical LTP (cLTP) and find that under these conditions, translocation is persistent. Using red fluorescent protein as a cell morphology marker, we found that there are two components of the persistent accumulation. cLTP produces a persistent increase in spine volume, and some of the increase in GFP-CaMKIIα is secondary to this volume change. In addition, cLTP results in a dramatic increase in the bound fraction of GFP-CaMKIIα in spines. To further study the bound pool, immunogold electron microscopy was used to measure CaMKIIα in the postsynaptic density (PSD), an important regulator of synaptic function. cLTP produced a persistent increase in the PSD-associated pool of CaMKIIα. These results are consistent with the hypothesis that CaMKIIα accumulation at synapses is a memory trace of past synaptic activity.en
dc.description.sponsorshipThis work was supported by Grant R01 NS-27337 from the National Institutes of Health/National Institute of Neurological Disorders and Stroke.en
dc.format.mimetypeapplication/pdf
dc.language.isoen_USen
dc.publisherSociety for Neuroscienceen
dc.relation.urihttps://doi.org/10.1523/JNEUROSCI.2350-04.2004
dc.subjectProtein kinaseen
dc.subjectPostsynaptic densityen
dc.subjectImagingen
dc.subjectSynapseen
dc.subjectLTP long-term potentiationen
dc.subjectEMen
dc.subjectTissue cultureen
dc.subjectFluorescenceen
dc.titlePersistent accumulation of calcium/calmodulin-dependent protein kinase II in dendritic spines after induction of NMDA receptor-dependent chemical long-term potentiationen
dc.typeArticleen
dc.identifier.doi10.1523/JNEUROSCI.2350-04.2004


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