Gene expression patterns in visual cortex during the critical period: Synaptic stabilization and reversal by visual deprivation

Abstract

The 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.actin ͉ myelin ͉ ocular dominance ͉ synaptic plasticity ͉ troponin

Transcriptomics of critical period of visual cortical plasticity in mice

“…Our data constitute a significant advance over available gene expression resources that use alternate methodologies (17). The advantages of RNA-seq over older methods, such as higher sensitivity and dynamic range, have been previously established by several authors (18,19).…”

Increased High-Sensitivity Troponin-T Levels Are Associated with Mortality After Ischemic Stroke

“…This specificity is present in early developmental stages in the embryo, where cardiac troponins are only expressed in beating heart tissue (Filipczyk et al 2007) and are mediated by a number of mechanisms, including specific promoters for cardiac troponin (Harlan et al 2008) and an amino acid sequence different from other troponin proteins (Akhter et al 2012). However, later in life, the troponin complex is prevalent in other tissues as well, and there is evidence suggesting that under certain conditions, genes encoding the cardiac troponin complex (type c) can undergo activation and be expressed even in the brain (Lyckman et al 2008). Furthermore, cardiac-specific troponin I has been shown to be expressed in non-small cell lung cancer cells (Chen et al 2014).…”

SynCAMs – From axon guidance to neurodevelopmental disorders

“…In contrast to other IgSF CAMs that stabilize LTP (longterm potentiation) and LTD, SynCAM1 prevents LTD without affecting LTP (Bukalo et al, 2004;Murai et al, 2002;Robbins et al, 2010). A role of SynCAM1 in synaptic plasticity was also demonstrated by its increased expression in the visual cortex after monocular deprivation (Lyckman et al, 2008).…”

“…SynCAM1 not only contributes to synaptogenesis, as it is required later in development for the maintenance of excitatory synapses and for the regulation of synaptic plasticity (Lyckman et al, 2008;Robbins et al, 2010). Overexpression of SynCAM1 abrogates loss of synapses during long-term depression (LTD) whereas loss of SynCAM1 increases LTD (Robbins et al, 2010).…”