Cyclosporin A (CsA) is an immunosuppressive drug used for organ transplant patients. Increased brain transport of CsA elevates the risk for the occurrence of neurotoxic adverse effects including seizures under the pathological conditions. However, it has not been well known which cell types composing brain tissue is the target for the occurrence of CsA-induced neurotoxicity. Brain pericytes located in brain microvessels is a key player in the development of neuroinflammation and blood-brain barrier (BBB) dysfunction under the pathological conditions, which implicated in brain dysfunction including seizures characterized by neuronal hyperexcitability. We therefore hypothesized that CsA stimulates brain pericytes to release mediators associated with BBB dysfunction and neuroinflammation. In this study, brain pericytes obtained from rat brains were incubated with CsA (1-10 μM) for 24 h. CsA treatment significantly increased the release of matrix metalloproteinase-9, a down-regulator of BBB function, from brain pericytes. Furthermore, CsA-treated pericytes showed elevated expressions of the inflammatory mediators, IL-6 and MCP-1. These findings suggested that brain pericytes may be a key player in the occurrence of CsA-induced neuronal adverse effects.