The mitochondrion serves many functions in the central nervous system (CNS) and other organs beyond the well-recognized role of adenosine triphosphate (ATP) production.This includes calcium-dependent cell signaling,regulation of gene expression,synthesis and release of cytotoxic reactive oxygen species,and the release of cytochrome c and other apoptotic cell death factors.Traumatic injury to the CNS results in a rapid and,in some cases,sustained loss of mitochondrial function.One consequence of compromised mitochondrial function is induction of the mitochondrial permeability transition (mPT) state due to formation of the cyclosporine A sensitive permeability transition pore (mPTP).In this mini-review,we summarize evidence supporting the involvement of the mPTP as a mediator of mitochondrial and cellular demise following CNS traumatic injury and discuss the beneficial effects and limitations of the current experimental strategies targeting the mPTP.