My dissertation research focused on the novel localization and subsequent characterization of a calpain (mu-calpain) to the mitochondria in cells of the central nervous system. Calpains are calcium dependent cysteine proteases that play a role in a number of physiological conditions including cell motility and cell division, however the hyperactivation of calpains can lead to pathological conditions and necrotic cell death. This phenomena is most readily evident in traumatic brain and spinal cord injury, where calpains are activated making the discovery of its mitochondrial localization of vital interest to the calpimmediately after injury and remain elevated for 24 hours post injury. The mitochondria are major cellular checkpoints for both programmed and non-programmed cell death or necrosis. Thus, the localization of a calpain to the mitochondria intruduces a number of injury paradigms that will need to be adressed in any calpain inhibitory strategy ain field.