Together, the comparable fractional anisotropy and peri-infarct Iba-1 immunoreactivity in PBS- and C3a-treated mice, and the reduced expression of GFAP and increased fiber tract density in C3a-treated mice, support the conclusion that intranasal treatment with C3a in the postacute phase after stroke promotes functional recovery at least in part by modulating neuronal connectivity and astrocyte reactivity. This evidence concerns the gene GFAP and stroke disorder.