Experience-Dependent Gene Expression in Adult Visual Cortex

J Chen,C D Gilbert,H Yamahachi

doi:10.1093/cercor/bhp131

J Chen, C D Gilbert + Show 1 more

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https://doi.org/10.1093/cercor/bhp131

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Abstract

Experience-dependent plasticity of the adult visual cortex underlies perceptual learning and recovery of function following central nervous system lesions. To reveal the signal transduction cascades involved in adult cortical plasticity, we utilized a model of remapping of cortical topography following binocular retinal lesions. In this model, the lesion projection zone (LPZ) of primary visual cortex (V1) recovers visually driven activity by the sprouting of horizontal axonal connections originating from the cells in the surrounding region. To explore the molecular mechanism underlying this process, we used gene microarrays from an expression library prepared from Macaque V1. By microarray analysis of gene expression levels in the LPZ and the surrounding region, and subsequent confirmation with Quantitative Real-Time polymerase chain reaction and in situ hybridization, the participation of a number of genes was observed, including the Rho GTPase family. Its role in regulation of cytoskeleton assembly provides a possible link between the alteration of neural activity and cortical functional reorganization.

Highlights

Experience-dependent plasticity of the adult visual cortex underlies perceptual learning and recovery of function following central nervous system lesions
Microarrays Identified Differentially Expressed Genes after Retinal Lesions To explore the patterns of gene expression associated with cortical reorganization, we employed the model of remapping of visual topography following retinal lesions
Functional recovery of visual cortex following retinal lesions provides an ideal model for revealing signal transduction pathways involved in adult cortical plasticity

Summary

Introduction

Experience-dependent plasticity of the adult visual cortex underlies perceptual learning and recovery of function following central nervous system lesions. Electrophysiological mapping has shown that the size of LPZ shrinks over time and recovers its ability to respond to visual stimuli, where the new input arises from parts of the retina surrounding the lesion (Gilbert et al 1990; Kaas et al 1990; Heinen and Skavenski 1991; Chino et al 1992; Gilbert and Wiesel 1992; Calford et al 2000) The circuitry underlying this recovery includes the plexus of long-range horizontal connections, which mediate a lateral spread of visual information within each cortical area (Darian-Smith and Gilbert 1995). To determine the signal transduction mechanisms underlying the sprouting of horizontal connections and the consequent remapping of cortical topography following retinal

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