Focal cerebral ischemia causes two temporal waves of Akt activation

We studied whether pro-survival Akt was activated after transient focal cer ebral ischemia and whether it inhibited pro-apoptotic Bad. Phosphorylation of Akt (serine-473) was enhanced in cortex after 1-hour ischemia, and also after 1 h and 6 h of reperfusion, but it returned back to that in controls by 24 h. After this first wave of Akt activation, a second increase was obs erved between 4 and 7 days. In striatum, only the late Akt activation was s een. In contrast to Akt, no Bad phosphorylation (serine-136) was detected a fter ischemia. Therefore, injury spontaneously activated Akt, but this did not suppress Bad signalling. It is proposed that further pharmacological ac tivation of Akt shortly after ischemia might promote cell survival, whereas Akt activation at longer time points is involved with glial reactivity. Ne uroReport 12:3381-3384 (C) 2001 Lippincott Williams & Wilkins.