Increased Expression of nNos Following Cortical Spreading Depression in Rat Brain

In our previous study, a prolonged period (48 h) of cortical spreading depression (CSD) effectively induced resistance to focal ischemia in 12 days without affecting rCBF, and significantly reduced the volume of infarcted lesion in rats, a phenomenon called `infarct tolerance’ [1]. Recently, NOS has been implicated in the decrease of hydroxyl radical (OH) generation following oxidative stress, via NO production as an antioxidant defense mechanism [2]. To analyze the role of the antioxidant defense mechanism via NO, the expression of neuronal nitric oxide synthase (nNOS) was examined following a prolonged period of CSD in rat neo-cortex.