The primary visual cortex (V1) has often been used as a model system to understand synaptic plasticity within intact cortical circuits. During the "critical period" of early development, V1 is extremely sensitive to changes in activity, such that brief manipulations in visual input cause functional changes in visually driven responses together with alterations in the structure of synapses on individual neurons and of connections between neurons. Structural changes at the level of dendritic spines - specialized F-actin rich protrusions on dendrites that receive the majority of excitatory input - are thought to underlie synaptic development and plasticity. In part, the Rho-family GTPase, Rac1, regulates the formation of spines and changes in their morphology. In this study we examined the correlation between structural changes in spines and Rac1 expression and activity. First, we monitored the expression level of proteins thought to regulate spine formation, such as spine-associated proteins (PSD95, GluR1) and Rac-signaling proteins (Rac, PAK, Actin). Critical period mice, aged ca P28, that were monocularly deprived (MD) for two days showed an increase in Rac1 expression in V1 contralateral to the lid suture. However, no difference in PSD95, GluR1, PAK, or beta actin expression was observed in immunoblotting or immunohistochemical analysis. Next, we examined the role of Rac in regulating the structure of spines and dendrites on V1 neurons before and after MD. A herpes simplex virus expressing two separate gene products, dsRed2 red fluorescent protein (RFP) and mutant Rac1 (constitutively active CA-Rac, or dominant negative DN-Rac), were expressed in critical period mice. The number and spine type (mushroom, stubby, or filopodia) was determined by measuring RFP-filled dendrites. After 4 days of expression, mutant Rac1 constructs altered number and class of spine type, thereby suggesting a role for Rac in structural changes at synapses during visual cortex plasticity.