In a model of ischemic stroke induced by photothrombosis - which results in ischemic lesion with minimal or no penumbra, and thus allows to study the effects of C3aR signaling on neural plasticity and functional recovery independent of neuroprotection - we showed that C3a overexpression in the GFAP-C3a mice increased whereas C3aR deficiency decreased the number of newly born neurons in the peri-infarct region on day 21 after stroke despite comparable infarct volumes [80]. This evidence concerns the gene GFAP and Stroke.