, 2005). Considering the two studies mentioned above, the present report appears to be one of the few to observe astrocytic plasticity after exercise, as we demonstrated increases of GFAP after 3 and 15 days of moderate exercise. We also detected an exercise-induced increase Androgen Receptor Antagonist concentration of cell proliferation and neurogenesis in the SGZ after all periods of exercise, and demonstrated that 3 days of moderate intensity treadmill exercise were sufficient to induce these changes. The immunostaining for DCX, a protein that promotes microtubule polymerization and is present in migrating neuroblasts and young neurons (von Bohlen Und Halbach, 2007), revealed increases that progressed
with exercise exposure. This finding suggests that even though the levels of cell proliferation remained stable through time, the ratio of cell differentiation possibly shifted towards the neuronal fate. Voluntary exercise has been shown to enhance neurogenesis and improve cognitive performance (Fabel and Kempermann, 2008 and van Praag, 2008). Other
authors have also reported increased neurogenesis after 3 days of exercise, but they do not comment on the distance their mice ran per night, therefore limiting possible comparisons to our results with rats (Kronenberg et al., 2006). In conclusion, the changes of SYN, NF68, GluR1, MAP2 and GFAP as a result of different periods of treadmill running reported here suggest a positive effect of short-term, moderate intensity treadmill exercise on hippocampal selleck compound plasticity, which was in general independent of transcription regulation and of BDNF upregulation. In addition, the present protocol appeared to be sufficient to increase hippocampal neurogenesis as early as 3 days
after exercise training. These changes might be subjacent to anatomical and functional plasticity of the hippocampal area generated by physical exercise. Furthermore, the increasing body of information on exercise-induced changes may be useful to develop strategies to prevent or treat functional decline following aging, neurological disorders and trauma. Male 2 month-old Wistar Decitabine order rats weighing ca. 250 g (obtained from the Animal Facility of the Institute of Biomedical Sciences of the University of São Paulo) were housed in groups in standard polyethylene cages with food and water ad libitum, room temperature of 23 °C and a 12/12 h light–dark inverted cycle ( Holmes et al., 2004). All protocols were approved by the Ethics Committee for Animal Research of the University of São Paulo and experimental procedures were performed in accordance with the guidelines of the Brazilian College for Animal Experimentation (COBEA) and the animal care guidelines of the National Institutes of Health (NIH/USA). All animals went through a two-day adaptation period to a treadmill (KT 3000 — IMBRAMED, Brazil, adapted for rats) during which they were allowed to explore the equipment and the treadmill was turned on for only 15 min at low speeds (0.3 to 0.5 km/h).