期刊
JOURNAL OF NEUROCHEMISTRY
卷 101, 期 1, 页码 232-240出版社
WILEY
DOI: 10.1111/j.1471-4159.2006.04360.x
关键词
estrogen; N-methyl-D-aspartate; phosphorylation; plasticity; signaling pathways; synaptoneurosome
资金
- NIA NIH HHS [P01 AG014751, AG14751] Funding Source: Medline
In addition to its well-known activational mechanism, the steroid hormone 17-beta-estradiol (E2) has been shown to rapidly activate various signal transduction pathways that could participate in estrogen-mediated regulation of synaptic plasticity. Although the mechanisms underlying these effects are not clearly understood, it has been repeatedly suggested that they involve a plasma membrane receptor which has direct links to several intracellular signaling cascades. To further address the question of whether E2 acts directly at the synapse and through membrane-bound receptors, we studied the effects of E2 and of ligands of estrogen receptors on various signaling pathways in cortical synaptoneurosomes. Our results demonstrate that E2 elicits N-methyl-D-aspartate receptor phosphorylation and activates the extracellular signal-regulated kinase and the phosphatidylinositol 3-kinase/Akt signal transduction pathways in this cortical membrane preparation. Furthermore, we provide evidence for the presence of a membrane-bound estrogen receptor responsible for these effects in cortical synaptoneurosomes. Our study demonstrates that E2 directly acts at cortical synapses, and that synaptoneurosomes provide a useful system to investigate the mechanisms by which E2 regulates synaptic transmission and plasticity.
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