After a transient increase in the expression of both nNOS and eNOS in the ischemic area, a secondary wave of NO overproduction starts to develop several hours after the initial ischemic insult and is sustained for up to 4–7 days [46,47] iNOS expression is much more variable in experimental stroke, as it may start around 4 hrs after MCAo [48] and 12 hrs after ischemia/reperfusion insult in transient forebrain ischemia model [49]. Here, NOS1 is linked to stroke disorder.