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Neural Plasticity
Volume 2012 (2012), Article ID 250421, 10 pages
http://dx.doi.org/10.1155/2012/250421
Research Article

IGF-1 Restores Visual Cortex Plasticity in Adult Life by Reducing Local GABA Levels

1Laboratory of Neurobiology, Scuola Normale Superiore, Piazza dei Cavalieri 7, 56100 Pisa, Italy
2Institute of Neuroscience, CNR, Via Moruzzi 1, 56100 Pisa, Italy
3Neuroscience Centre, University of Helsinki, 00014 Helsinki, Finland

Received 10 February 2012; Accepted 1 April 2012

Academic Editor: Małgorzata Kossut

Copyright © 2012 José Fernando Maya-Vetencourt et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The central nervous system architecture is markedly modified by sensory experience during early life, but a decline of plasticity occurs with age. Recent studies have challenged this dogma providing evidence that both pharmacological treatments and paradigms based on the manipulation of environmental stimulation levels can be successfully employed as strategies for enhancing plasticity in the adult nervous system. Insulin-like growth factor 1 (IGF-1) is a peptide implicated in prenatal and postnatal phases of brain development such as neurogenesis, neuronal differentiation, synaptogenesis, and experience-dependent plasticity. Here, using the visual system as a paradigmatic model, we report that IGF-1 reactivates neural plasticity in the adult brain. Exogenous administration of IGF-1 in the adult visual cortex, indeed, restores the susceptibility of cortical neurons to monocular deprivation and promotes the recovery of normal visual functions in adult amblyopic animals. These effects were accompanied by a marked reduction of intracortical GABA levels. Moreover, we show that a transitory increase of IGF-1 expression is associated to the plasticity reinstatement induced by environmental enrichment (EE) and that blocking IGF-1 action by means of the IGF-1 receptor antagonist JB1 prevents EE effects on plasticity processes.