Additionally, the immunocontent of hippocampal glutamine synthetase (GS) was not affected by KA-induced seizures at any time point investigated ( Fig. 3). As the hippocampal glutamate uptake and the immunocontent of astrocytic (GLT1 and GLAST) glutamate transporters were modified in the hippocampus 24 h after the end of seizures episode, immunohistochemical analysis for GFAP, NeuN and DAPI was performed in this time in all subfields of the hippocampus [CA1, CA3 and dentate gyrus (DG)]. There was an increase in the GFAP immunoreactivity in KA group as compared to control group in

all subfields (Fig. 4). In the regions surrounding pyramidal layer (SPL) SAHA HDAC clinical trial and over pyramidal layer (PL) of CA3 there was an increase of 147% and 100% for GFAP immunoreactivity compared to control group, respectively (Fig. 4; first panel). Likewise, surrounding pyramidal layer (SPL) and over pyramidal layer (PL) of CA1 there was an increase of 100% and 40% for GFAP immunoreactivity compared to control group, respectively (Fig. 4; second panel). GFAP immunoreactivity increased 100% compared to saline-treated rats in the dentate gyrus (DG) (Fig. 4; third panel). NeuN immunoreactivity

and DAPI staining were similar between both groups, indicating absence of neuronal loss 24 h after seizure (data not shown). Sixty days after the seizures episode, male rats were submitted to behavioral Linsitinib manufacturer tasks. In elevated plus-maze task, aiming to assess anxiety-related behavior (Fig. 5), kainate-treated rats presented a decrease on the time spent and the number of entries in open arms compared to saline-treated rats (Fig. 5). Kainate-treatment abolished the short- (1.5 h after training) and long- (24 h after training) term memory, evaluated in an inhibitory avoidance task (Fig. 6). The present study shows

that rats presenting KA-induced seizures in early periods of development presented see more brain acute molecular and biochemical alterations related to the glutamatergic system, and long-term behavioral impairment in adulthood. The short-term effects investigated were on hippocampal glutamate uptake and on astrocytic glutamate transporters immunocontent. At 12 h after seizures, there was an increase in the glutamate uptake (that did not reach statistical significance) and in both GLT-1 and GLAST immunocontent. At 24 h after seizures, the GLAST levels remained up regulated, while the glutamate uptake activity and the GLT-1 levels became diminished. The EAAC1 and glutamine synthetase levels did not vary. Based upon the common pattern of temporal adaptation, GLT-1 seems to be responsible for the transient increase and further decrease on glutamate uptake observed in the hippocampus obtained 12 and 24 h after the end of seizures, respectively.