To determine whether the increase in newborn neurons induced by IL-17 A during stroke recovery properly integrates into the striatal network, synaptogenesis markers SNAP-25 and Synaptophysin were used as indices and outcome measures for synaptogenesis at 35 d.p.i.18, 19 WT mice showed higher Synaptophysin and SNAP-25 expression in the ischemic boundary zone (IBZ) compared with il-17a−/− mice; anti-IL-17 A mAb treatment also significantly decreased the Synaptophysin and SNAP-25 expression, whereas rIL-17 A conferred the opposite effects (Figures 3c–f). This evidence concerns the gene SNAP25 and stroke disorder.