Abstract：
:Transient global ischemia induces selective, delayed neuronal death of pyramidal neurons in the hippocampal CA1. Whereas long term treatment of middle-aged female rats with estradiol at physiological doses ameliorates neuronal death, the signaling pathways that mediate the neuroprotection are, as yet, unknown. Protein kinase B (Akt) and downstream transcription factors, the cAMP response element binding protein (CREB) and signal transducer and activator of transcription (STAT3) are critical players in cellular survival following injury. The present study was undertaken to determine whether long term estradiol alters the phosphorylation status and activity of Akt, STAT3 and CREB in ovariohysterectomized, middle-aged and young female rats subjected to global ischemia. Irrespective of either hormone or ischemic condition, middle-aged females exhibited lower levels of p-CREB and higher levels of Akt and STAT3 in CA1 than young females, as assessed by Western blot. In middle-aged animals, ischemia increased the phosphorylation status/activity of Akt and STAT3, and decreased the phosphorylation status/activity of CREB in the hippocampal CA1. Whereas estradiol did not detectably alter the phosphorylation status/activity of Akt or STAT3, it prevented the ischemia-induced decrease in nuclear p-CREB. Similar results were observed for the young females. Collectively, these data demonstrate that CREB, STAT3, and Akt are involved in the molecular response to global ischemia and that age influences the status of CREB, STAT3 and Akt activity in CA1 under physiological as well as pathological conditions, further emphasizing the importance of including older rodents in neuroprotection studies.
journal_name
Brain Resjournal_title
Brain researchauthors
De Butte-Smith M,Zukin RS,Etgen AMdoi
10.1016/j.brainres.2012.06.036subject
Has Abstractpub_date
2012-08-30 00:00:00pages
118-28eissn
0006-8993issn
1872-6240pii
S0006-8993(12)01111-0journal_volume
1471pub_type
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