Skip to main content
. Author manuscript; available in PMC: 2011 Jan 27.
Published in final edited form as: Steroids. 2009 Jan 20;74(7):555–561. doi: 10.1016/j.steroids.2009.01.003

Figure 3. Long-term estradiol treatment blunts ischemia-induced ERK1 dephosphorylation and acts via MAPK to prevent ischemia-induced CREB dephosphorylation.

Figure 3

Animals were treated as described in Figure 2. They were infused icv with vehicle or the MEK inhibitor PD98059 immediately after reperfusion, killed 1 or 3 h later, and the hippocampal CA1 microdissected. Total cell lysates or nuclear fractions were immunoblotted for total and phospho- (p) ERK-1 and CREB. (A) Ischemia induced dephosphorylation of ERK1 at 1 h after global ischemia. Estradiol significantly increased basal p-ERK1 in shams and maintained levels of p-ERK1 in ischemic rats at 1h. PD98059 reversed the ability of estradiol to maintain p-ERK1 in postischemic CA1. (B) Ischemia promoted dephosphorylation of CREB in the nuclei of CA1 neurons. Estradiol maintained the phosphorylated, activated state of CREB in the CA1 of ischemic rats. PD98059 blocked the ability of estradiol to maintain p-CREB levels in postischemic CA1. Data are from Jover-Mengual et al., 2007.

*, P<0.05; **, P<0.01.