Gene expression changes and molecular pathways mediating activity-dependent plasticity in visual cortex.
Nat Neurosci, 2006/5;9(5):660-8.
Tropea D[1], Kreiman G, Lyckman A, Mukherjee S, Yu H, Horng S, Sur M
Affiliations
PMID: 16633343
Impact factor: 28.771
Abstract
Two key models for examining activity-dependent development of primary visual cortex (V1) involve either reduction of activity in both eyes via dark-rearing (DR) or imbalance of activity between the two eyes via monocular deprivation (MD). Combining DNA microarray analysis with computational approaches, RT-PCR, immunohistochemistry and physiological imaging, we find that DR leads to (i) upregulation of genes subserving synaptic transmission and electrical activity, consistent with a coordinated response of cortical neurons to reduction of visual drive, and (ii) downregulation of parvalbumin expression, implicating parvalbumin-expressing interneurons as underlying the delay in cortical maturation after DR. MD partially activates homeostatic mechanisms but differentially upregulates molecular pathways related to growth factors and neuronal degeneration, consistent with reorganization of connections after MD. Expression of a binding protein of insulin-like growth factor-1 (IGF1) is highly upregulated after MD, and exogenous application of IGF1 prevents the physiological effects of MD on ocular dominance plasticity examined in vivo.
MeSH terms
Animals; Animals, Newborn; Darkness; Gene Expression Regulation; Immunohistochemistry; Mice; Nerve Tissue Proteins; Neuronal Plasticity; Oligonucleotide Array Sequence Analysis; RNA, Messenger; Reverse Transcriptase Polymerase Chain Reaction; Sensory Deprivation; Signal Transduction; Vision, Binocular; Vision, Monocular; Visual Cortex; Visual Pathways
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