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. 2001 Dec 1;21(23):9204–9213. doi: 10.1523/JNEUROSCI.21-23-09204.2001

Fig. 3.

Fig. 3.

CREB phosphorylation and ischemic tolerance induced after sublethal stress were inhibited by MK801. Effects of the length of ischemia and NMDA receptor antagonist MK801 on CREB phosphorylation after reperfusion for 15 min (A, B).A, Western blot analyses of proteins extracted from the gerbil hippocampus after reperfusion for 15 min after transient forebrain ischemia for 1, 2, or 5 min (top panel). The bar graph (bottom panel) is presented as fold increase in pCREB levels after global ischemia. There was no enhancement of CREB phosphorylation after 1 min of ischemia, whereas both 2 and 5 min of ischemia induced significant increase in pCREB levels. Each column and bar represents the mean ± SD (n = 7 for each ischemic period); *p < 0.05 versus sham-operated animals.B, Intraperitoneal administration of MK801 60 min before transient forebrain ischemia prevented CREB phosphorylation observed after ischemia-reperfusion (n = 3 each).C, Intraperitoneal administration of MK801 before 2 min of preconditioning ischemia abolished neuronal protection. Ischemic tolerance was induced by 2 min of ischemia 4 d before 5 min of ischemia. Each column and bar represents the mean ± SD of neuronal density in the CA1 (n = 6 for each experiment). *p < 0.05 versus all other groups with 5 min of ischemia.