, 2005, Bury and Jones, 2002, Conner

et al., 2003, Grabowski et al., 1993 and Zai et al., 2009). We have previously shown sensorimotor recovery of impaired forelimb after treatment with LDK378 chemical structure BMMCs in a model of unilateral focal cortical ischemia. We used functional tests that do not require training and evaluate unsophisticated forelimb movements (de Vasconcelos dos Santos et al., 2010 and Giraldi-Guimarães et al., 2009), i.e., cylinder and adhesive tests (Schaar et al., 2010 and Schallert, 2006). Here, we extended the functional analysis of the same model of ischemia using the “reaching chamber/pellet retrieval” (RCPR) task (Schaar et al., 2010). We evaluated the effectiveness of the BMMCs treatment on the skilled movement of grasping with forepaw after unilateral focal cortical ischemia. Furthermore, skilled training has been shown to promote cortical motor map reorganization and enhancement of lesion-induced structural plasticity in motor cortex (Jones et al., 1999, Kleim et al., 1998 and Kleim et al., 2004). Since the RCPR task involves pre-ischemic training and a high frequency of testing after ischemia, we also evaluated a possible effect of the RCPR training,

alone and associated to the BMMCs treatment, on the performance in sensorimotor tests previously studied PD-0332991 order in the same model of ischemia (de Vasconcelos dos Santos et al., 2010 and Giraldi-Guimarães et al., 2009). The protocol of cortical ischemia by thermocoagulation has been shown to induce a focal lesion subjacent to the affected submeningeal blood vessels, including the six cortical layers and sparing the white matter (de Vasconcelos dos Santos et al., 2010, Giraldi-Guimarães et al., 2009 and Szele et al., 1995). This model of lesion is induced by heat, and a limited

thermal Chloroambucil effect could not be discharged, especially in most superficial cortical layers (Riban and Chesselet, 2006). Given that tissue damage induced by thermal effect should be faster than by ischemia, we analyzed the presence of cortical lesion after a short time window. Reaction with TTC of brain sections from ischemic animals sacrificed 1 h after thermocoagulation revealed slight tissue loss in the cortical surface (Fig. 2A). It could be induced by thermal damage, although an initial degeneration promoted by the ischemic process cannot be ruled out. This result indicated that the thermal effect should be restricted to the cortical surface immediately behind the meninges and represented a minimal component of the cortical lesion induced by thermocoagulation. Three days after ischemia, a clear focal cortical lesion was revealed by TTC reaction (Fig. 2B), in accordance to previous descriptions (de Vasconcelos dos Santos et al., 2010, Giraldi-Guimarães et al., 2009 and Szele et al., 1995).