, 1995) and promotes survival and growth

of neurons (Anderson et al., 1988), all of which are increased by exercise (Black et al., 1990, Li et al., 2005 and van Praag et al., 1999b). Another candidate to participate in the regulation of the above mentioned plastic mechanisms is the epidermal growth factor (EGF). Although EGF has been shown to promote survival and differentiation of postmitotic neurons (Morrison et al., 1987) and to increase the density of newborn cells in the subventricular zone, it appears to shift the ratio of differentiation of those cells towards a glial lineage in the SGZ (Kuhn et al., 1997), whereas we observed a shift towards the neuronal fate based check details on the increase of DCX-positive cells. On the other hand, EGF might have played some role in exercise-induced hippocampal plasticity observed here, as we detected increased GFAP levels, and EGF is known to induce proliferation of astrocytes (Kornblum et al., 1998). Alternatively, it is possible that BDNF signaling is increased by the present protocol through receptor sensitization/upregulation, which remains to be evaluated. BDNF is involved

in the synthesis (Vaynman et al., 2006) and phosphorylation of SYN (Jovanovic et al., 1996 and Jovanovic et al., 2000). Even though we found BDNF levels to be unchanged after the present protocol of exercise, we observed increased levels of SYN at EX7. SYN is involved in vesicle learn more clustering, neurotransmitter release, axonal elongation and maintenance of synaptic contacts (Fornasiero et al., 2010, Greengard et al., 1993 and Jovanovic et al., 1996). This synaptic protein is frequently used as a predictor of synaptic density (De Immune system Camilli et al., 1983 and Fornasiero et al., 2010) and is increased by exercise (Molteni

et al., 2002 and Vaynman et al., 2006). These studies, as well as many others, support our findings of increased SYN after exercise. We did not notice, however, changes of SYP, the second nerve terminal protein studied here, even though this protein has been noted to change in the same proportion as SYN after some exercise protocols (Vaynman et al., 2006). As mentioned earlier, exercise increases glutamatergic activity (Leung et al., 2006). Glutamate is definitely involved in the mechanisms that promote learning and memory, and the activation of glutamate receptors has a role in the generation of LTP as a response to exercise (van Praag et al., 1999a). GluR1 and GluR2 are clearly related to LTP mechanisms and do undergo plastic changes after exercise (Dietrich et al., 2005 and Real et al., 2010). Since it has been shown that short-term exercise promotes an increase of glutamate (Leung et al., 2006), the decreased levels of GluR1 at EX3 observed in our study could represent a protective strategy to prevent over-excitation and neurotoxicity by glutamate.