Impaired glutamate uptake and lowered expression of glutamate transporter (excitatory amino acid transporter: EAAT) in activated astrocytes are involved in the development of neuronal hyperexcitability in traumatic brain injury (TBI). Our previous study showed that astrocytic activation, characterized by increased GFAP expression, is preceded by increased expression of platelet-derived growth factor receptor (PDGFR) β in brain pericytes of TBI mice. However, little is known about the role of pericyte in dysregulation of glutamate uptake via EAAT in astrocytes under TBI pathology. Here, we investigated whether reactive pericytes in the early phase after TBI modulate EAAT2 expression in astrocytes. EAAT2 expression in astrocytes was significantly lower in the ipsilateral hippocampus 28 days after TBI than after sham operation. The decreased EAAT2 levels in TBI mice on postoperative day 28 were reversed by treatment with imatinib, a PDGFRβ inhibitor, during a period of postoperative day 0–4. In this period, PDGFRβ expression was increased in pericytes. These findings suggest that increased PDGFRβ expression in pericytes in the early phase causes the downregulation of EAAT2 expression in astrocytes in the late phase after TBI and drives the development of impaired glutamate uptake in astrocytes after TBI.