By using Fluoro-Jade C (FJC) staining in brain sections, a large number of degenerative neuronal cells were observed in brains from SE group (Fig. 1). The FJC-positive staining cells showed a bright green color in the selleck kinase inhibitor somas and fine processes with neuronal profiles (Fig. 1 inserts). LiCl–pilocarpine administration induced a massive neurodegeneration in several brain regions, including CA1 hippocampal subfield, habenula (lateral habenular nucleus), thalamus (ventral posteromedial thalamic nucleus) and amygdala (medial amygdaloid nucleus) 24 h after SE onset (Fig. 1). Both ketamine post-SE onset treated groups presented a significant reduction in the number of FJC-positive neurons (85–100%)
in all brain regions
analyzed (Table 1). FJC-positive neurons were not observed in brain regions from control (CTRL) and KET groups. The pattern of distance traveled, and number of animals rearing and grooming across time were similar in all groups (Fig. 2A–C). All animals showed intra-session habituation SCH772984 cell line to apparatus approximately 7 min after the starting of the session. There were no differences in other parameters of locomotor and exploratory activities, temporal organization and spatial distribution in all groups (Fig. 2D–F and supplementary Fig. S1 A–F). Moreover, all groups showed a similar pattern of inter-session habituation of the distance traveled, and number of animals rearing and grooming during the three days of testing (data not shown). Animals from SE and KET groups spent significantly low time in open arms (62.9±16.8 and 40.1±6.9, respectively; F=6.626; p=0.0004) when compared to the CTRL group (150.1±10.3) ( Fig. 3A). Ketamine post-SE onset treatment in both times (SE+KET15 and SE+KET60) increased the time spent in open arms
(115.9±15.3 and 101.5±19.2, respectively), however these values were not different from both CTRL and SE groups. SE+KET15 and SE+KET60 groups, when compared with only KET, spent more time in open arms. The number of risk assessment behaviors was significantly increased in the KET group (7.3±1.4) when compared to the CTRL and SE+KET60 groups (2.8±0.6 and 2.6±0.6, respectively) ( Fig. 3B; F=4.679; p=0.0038). Animals from SE (7.0±1.4), SE+KET15 (4.1±0.9), SE+KET60 and CTRL groups presented similar levels of risk assessment Quisqualic acid behaviors. All groups presented similar number of total entries in both open and closed arms ( Fig. 3C; F=2.262; p=0.0816). SE when occurred during brain development may cause acute neurodegeneration followed by behavioral and cognitive deficits later in life (Holmes, 1997 and van Esch et al., 1996). The acute neuronal loss induced by SE is associated with NMDAR-mediated glutamatergic excitotoxicity whereas several studies have reported that pretreatments with NMDAR antagonists are effective in preventing neuronal damage (Clifford et al., 1990, Fariello et al.