These studies originated the idea that although under non-ischemic conditions tPA is pivotal for neurophysiological processes required for normal brain function such as neurite outgrowth (Krystosek and Seeds, 1981), learning (Seeds et al., 2003) and memory (Baranes et al., 1998), during cerebral ischemia it plays a completely opposite role as a mediator of excitotoxin-induced neuronal death. Here, PLAT is linked to brain ischemia.