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dc.contributor.authorVan Wart, Audraen
dc.contributor.authorLyckman, Alvin W.en
dc.contributor.authorHorng, Samen
dc.contributor.authorLeamey, Catherine A.en
dc.contributor.authorTropea, Danielaen
dc.contributor.authorWatakabe, Akiyaen
dc.contributor.authorMcCurry, Cortinaen
dc.contributor.authorYamamori, Tetsuoen
dc.contributor.authorSur, Mrigankaen
dc.description.abstractThe mapping of eye-specific, geniculocortical inputs to primary visual cortex (V1) is highly sensitive to the balance of correlated activity between the two eyes during a restricted postnatal critical period for ocular dominance plasticity. This critical period is likely to have amplified expression of genes and proteins that mediate synaptic plasticity. DNA microarray analysis of transcription in mouse V1 before, during, and after the critical period identified 31 genes that were up-regulated and 22 that were down-regulated during the critical period. The highest-ranked up-regulated gene, cardiac troponin C, codes for a neuronal calcium-binding protein that regulates actin binding and whose expression is activity-dependent and relatively selective for layer-4 star pyramidal neurons. The highest-ranked down-regulated gene, synCAM, also has actin-based function. Actinbinding function, G protein signaling, transcription, and myelination are prominently represented in the critical period transcriptome. Monocular deprivation during the critical period reverses the expression of nearly all critical period genes. The profile of regulated genes suggests that synaptic stability is a principle driver of critical period gene expression and that alteration in visual activity drives homeostatic restoration of stability.en
dc.publisherNational Academy of Sciencesen
dc.subjectOcular dominanceen
dc.subjectSynaptic plasticityen
dc.titleGene expression patterns in visual cortex during the critical period: Synaptic stabilization and reversal by visual deprivationen
dc.typeArticle - Refereeden
dc.rights.holderCopyright 2008 National Academy of Sciencesen
dc.description.notespp. 9409-9414

This article contains supporting information online at 0710172105/DCSupplemental.

dc.title.serialProceedings of the National Academy of Sciences of the United States of Americaen

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