For testing, each animal was lowered into to the testing arena in which one familiar Ginsenoside-F2 object was replaced with a novel object. The animal was lowered into the arena, equidistant and facing away from each object. Each session was video record and the animal was given 5 min to explore. The time spent exploring each object was scored for each mouse from the video. Exploration was defined as the animal��s nose being within 2 cm of and pointed toward the object. Time during which the animal propped itself up on the object in order to explore higher levels of the arena was not considered exploration time for that object. The discrimination ratio was calculated as the time spent with the novel object divided by the total time spent exploring either object. Objects were randomized and counterbalanced across animals and groups. Objects and arenas were thoroughly cleaned with 70% ethanol between trials to prevent olfactory cues. Of note, the visual ability of each mouse was assessed by suspending the animal by the tail and slowly lowering it toward a sold dark surface for three successive trials. Visual acuity was demonstrated by the animal��s reaching for the surface before vibrissae made contact with it. All mice demonstrated full visual capability. Here, we explored the role of Terutroban miR132 in vivo using a bitransgenic tTA::miR132 mouse model, in which miR132 was over expressed in excitatory neurons throughout the forebrain. Using a thy1-GFP morphological marker, we demonstrated that in CA1 pyramidal neurons, transgenic miR132 induces an increase in dendrite spine density. This finding is consistent with recent work using cell culture and brain slice-based methodologies, which showed that miR132 increased spinogenesis. Further, the work of Impey et al. showed that miR132 regulates synapse formation and function, thus raising the possibility that overexpression of miR132 affects synaptic communication in vivo. Future studies will examine this question in detail. To test the functionality of transgenic miR132 at a molecular level, we examined the expression of MeCP2. Beyond simply validating the function of transgenic miR132, the data presented here, showing a down-regulation of MeCP2, has potentially significant ramifications for cognitive performance. MeCP2 is a multifunction protein that has been implicated in both the negative regulation of gene expression and RNA splicing. As noted above, dysregulation of MeCP2 is associated with neuronal developmental abnormalities in Rett Syndrome. Interestingly, in both Rett syndrome and in MeCP2-deficient mice, forebrain neurons exhibit a reduction in spine density. This effect is somewhat inconsistent with the increase in spine density observed in the miR132 mice.