Platelet‐derived growth factor receptor β (PDGFRβ) is upregulated after brain injury and its depletion results in the blood–brain barrier (BBB) damage. We investigated the time‐window and localization of PDGFRβ expression in mice with intrahippocampal kainic acid‐induced status epilepticus (SE) and in rats with lateral fluid‐percussion‐induced traumatic brain injury (TBI). Tissue immunohistochemistry was evaluated at several time‐points after SE and TBI. The distribution of PDGFRβ was analyzed, and its cell type‐specific expression was verified with double/triple‐labeling of astrocytes (GFAP), NG2 cells, and endothelial cells (RECA‐1). In normal mouse hippocampus, we found evenly distributed PDGFRβ+ parenchymal cells. In double‐labeling, all NG2+ and 40%–60% GFAP+ cells were PDGFRβ+. After SE, PDGFRβ+ cells clustered in the ipsilateral hilus (178% of that in controls at fourth day, 225% at seventh day, P < 0.05) and in CA3 (201% at seventh day, P < 0.05), but the total number of PDGFRβ+ cells was not altered. As in controls, PDGFRβ‐immunoreactivity was detected in parenchymal NG2+ and GFAP+ cells. We also observed PDGFRβ+ structural pericytes, detached reactive pericytes, and endothelial cells. After TBI, PDGFRβ+ cells clustered in the perilesional cortex and thalamus, particularly during the first post‐injury week. PDGFRβ immunopositivity was observed in NG2+ and GFAP+ cells, structural pericytes, detached reactive pericytes, and endothelial cells. In some animals, PDGFRβ vascular staining was observed around the cortical glial scar for up to 3 months. Our data revealed an acute accumulation of PDGFRβ+ BBB‐related cells in degenerating brain areas, which can be long lasting, suggesting an active role for PDGFRβ‐signaling in blood vessel and post‐injury tissue recovery. GLIA 2017;65:322–341