PT  - JOURNAL ARTICLE
AU  - Chiara Cerri
AU  - Alessia Fabbri
AU  - Eleonora Vannini
AU  - Maria Spolidoro
AU  - Mario Costa
AU  - Lamberto Maffei
AU  - Carla Fiorentini
AU  - Matteo Caleo
TI  - Activation of Rho GTPases Triggers Structural Remodeling and Functional Plasticity in the Adult Rat Visual Cortex
AID  - 10.1523/JNEUROSCI.2617-11.2011
DP  - 2011 Oct 19
TA  - The Journal of Neuroscience
PG  - 15163--15172
VI  - 31
IP  - 42
4099  - http://www.jneurosci.org/content/31/42/15163.short
4100  - http://www.jneurosci.org/content/31/42/15163.full
SO  - J. Neurosci.2011 Oct 19; 31
AB  - A classical example of age-dependent plasticity is ocular dominance (OD) plasticity, triggered by monocular deprivation (MD). Sensitivity of cortical circuits to a brief period of MD is maximal in juvenile animals and downregulated in adult age. It remains unclear whether a reduced potential for morphological remodeling underlies this downregulation of physiological plasticity in adulthood. Here we have tested whether stimulation of structural rearrangements is effective in promoting experience-dependent plasticity in adult age. We have exploited a bacterial protein toxin, cytotoxic necrotizing factor 1 (CNF1), that regulates actin dynamics and structure of neuronal processes via a persistent activation of Rho GTPases. Injection of CNF1 into the adult rat visual cortex triggered a long-lasting activation of the Rho GTPase Rac1, with a consequent increase in spine density and length in pyramidal neurons. Adult rats treated with CNF1, but not controls, showed an OD shift toward the open eye after MD. CNF1-mediated OD plasticity was selectively attributable to the enhancement of open-eye responses, whereas closed-eye inputs were unaffected. This effect correlated with an increased density of geniculocortical terminals in layer IV of monocularly deprived, CNF1-treated rats. Thus, Rho GTPase activation reinstates OD plasticity in the adult cortex via the potentiation of more active inputs from the open eye. These data establish a direct link between structural remodeling and functional plasticity and demonstrate a role for Rho GTPases in brain plasticity in vivo. The plasticizing effects of Rho GTPase activation may be exploited to promote brain repair.