05) and EX15 (p < 0.001) [F(3,28) = 14.64, p < 0.0001], accompanied by increased protein levels only at EX15 (p < 0.01) [F(3,28) = 7.019, p = 0.0012] (Fig. 2). Anti-GluR1 and anti-GluR2/3 stained perikarya and neuropil in the polymorphic layer, whereas some cells in the granular cell layer Erlotinib stained only for GluR1. We observed a decreased staining for GluR1

in the hilar region at all exercise periods (p < 0.001) with a more pronounced decrease at EX3 [F(3,28) = 39.11, p < 0.0001], which was the only group that presented decreased protein levels (p < 0.05) [F(3,28) = 4.046, p = 0.0165] (Fig. 3). As for GluR2/3, whereas protein changes were not detected [F(3,28) = 2.833, p = 0.0563], the staining pattern in the hilar region suggested increases at EX7 and EX15 (p < 0.05) [F(3,28) = 5.612, p = 0.0038] (Fig. 3). Anti-BDNF, on the other hand, stained mostly perikarya in the polymorphic and granular cell layers and, interestingly, neither the staining for BDNF [F(3,28) = 1.445, p = 0.2509] nor its protein levels [F(3,28) = 2.527, p = 0.0777] showed changes after the exercise protocol used here (Fig. 4). As for the real-time PCR analysis, we only observed an increase of MAP2 mRNA expression GSK-3 inhibitor at EX7 (p < 0.05) [F(3,28) = 4.788, p = 0.0081]. No changes

were observed for any of the other gene transcripts, and the expression of the GluR3 mRNA could not be detected in the hippocampus in our conditions. The results for the mRNA analysis are summarized in Table 1. In regard to cell proliferation and neurogenesis, we observed an increased number of BrdU-positive cells [F(3,20) = 25.39, p < 0.0001] and of DCX-positive

cells [F(3,20) = 24.99, p < 0.0001] in the SGZ at all exercise periods. The number of BrdU-positive cells reached a ca. 2-fold increase at EX3, was highest at EX7 and was still increased at EX15 (p < 0.001), although not as high as at EX3 and EX7 (Fig. 5). The staining for the neurogenesis marker DCX appeared to increase progressively 2-hydroxyphytanoyl-CoA lyase with exercise exposure and was found to be increased at all exercise periods (p < 0.001) (Fig. 5). We also verified the occurrence of SGZ neurons co-localizing BrdU and DCX (Fig. 6), as expected. The results of the corticosterone measurements revealed an increase of plasma levels at EX3 (ca. 73%, 3742 ± 431 pg/ml, p < 0.05) and at EX7 (ca. 174%, 5901 ± 721 pg/ml, p < 0.001), whereas the levels for EX15 (2678 ± 313 pg/ml) were similar to the levels detected in the sedentary group (2151 ± 276 pg/ml) [F(3,31) = 13.69, p < 0.0001], as previously reported (Real et al., 2010). The short-term exercise protocol used here appeared to induce increases of SYN, NF68, MAP2 and GFAP, accompanied by a decrease of GluR1. The only transcriptional effect detected was an increase of the mRNA coding for MAP2. The other proteins and mRNAs studied remained unchanged, whereas BrDU- and DCX-positive cells increased.