The mitochondrial permeability transition pore is an inducer of cell death. 
During the reperfusion phase after cerebral ischemia, calcium accumulates in 
mitochondria, and a burst of free radical formation occurs, conditions that 
favor the activation of the mitochondrial permeability transition pore. Here the 
authors demonstrate that a blocker of the mitochondrial permeability transition 
pore, the nonimmunosuppressive cyclosporin A analogue N-methyl-Val-4-cyclosporin 
A (10 mg/kg intraperitoneally), administered during reperfusion and at 24 hours 
of reperfusion, diminishes infarct size in a rat model of transient focal 
ischemia of 2 hours' duration. The mitochondrial permeability transition pore 
may be an important target for drugs against stroke.