While tissue plasminogen activator (tPA)-activated plasmin has been suggested to induce PAR1-mediated regulation of NMDA receptor function in a manner relevant for synaptic plasticity and behaviour [204,205], NMDA receptor activity seems to be necessary for thrombin/PAR1-induced neurodegenerative effects under pathological conditions such as ischemia or hemorrhage [206,207]. This evidence concerns the gene MARK2 and hemorrhage.