Journal
BRAIN RESEARCH
Volume 1379, Issue -, Pages 98-108Publisher
ELSEVIER
DOI: 10.1016/j.brainres.2010.07.053
Keywords
Reproductive senescence; Synapses; Dendritic spine; Electron microscopy; Akt; Signaling molecules
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Funding
- NIA NIH HHS [P01 AG016765, P01-AG16765] Funding Source: Medline
- NIDA NIH HHS [R01 DA008259, DA08259] Funding Source: Medline
- NINDS NIH HHS [NS07080, R01 NS007080] Funding Source: Medline
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The estrogen 17 beta-estradiol (E) increases the axospinous synaptic density and plasticity in the hippocampal CA1 region of young female rats but fails to do so in aged female rats. This E stimulus on synaptic plasticity is associated with the phosphorylation-dependent activation of Akt kinase. Our previous findings demonstrated that increased estrogen levels subsequently increase phosphorylated Akt (pAkt)-immunoreactivity (-IR) within the dendritic shafts and spines of pyramidal neurons in young female rats. Therefore, because Akt can promote cell survival and growth, we tested the hypothesis that the less plastic synapses of aged female rats would contain less E-stimulated pAkt-IR. Here, young (3-4 months) and aged (22-23 months) female rats were ovariectomized 7 days prior to a 48-h administration of either vehicle or E. The pAkt-IR synaptic distribution was then analyzed using post-embedding electron microscopy. In both young and aged rats, pAkt-IR was found in dendritic spines and terminals, and pAkt-IR was particularly abundant at the post-synaptic density. Quantitative analyses revealed that the percentage of pAkt-labeled synapses was significantly greater in young rats compared to aged rats. Nonetheless, E treatment significantly increased pAkt-IR in pre- and post-synaptic profiles of both young and aged rats, although the stimulus in young rats was notably more widespread. These data support the evidence that hormone-activated signaling associated with cell growth and survival is diminished in the aged brain. However, the observation that E can still increase pAkt-IR in aged synapses presents this signaling component as a candidate target for hormone replacement therapies. (C) 2010 Published by Elsevier B.V.
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