Nature Neuroscience 9, 660 - 668 (2006)
Published online: 23 April 2006; | doi:10.1038/nn1689
Gene expression changes and molecular pathways mediating activity-dependent plasticity in visual cortexDaniela Tropea1, Gabriel Kreiman2, Alvin Lyckman1, 3, Sayan Mukherjee2, 3, Hongbo Yu1, Sam Horng1
& Mriganka Sur11
Department of Brain and Cognitive Sciences and Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. 2
Department of Brain and Cognitive Sciences and McGovern Institute for Brain Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. 3
Present addresses: Tufts School of Medicine, Caritas St. Elizabeth's Medical Center, Center for Biomedical Research 406, 736 Cambridge Street, Brighton, Massachusetts 02135-2997, USA (A.L.); Institute for Genome Sciences and Policy, CIEMAS, Duke University, 101 Science Drive, Box 3382, Durham, North Carolina 27708, USA (S.M.).
Correspondence should be addressed to Mriganka Sur msur@mit.edu 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.
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