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Center for Reproductive Medicine and Infertility, Weill Medical College of Cornell University (J.M.C., Z.R.), New York, New York 10021; Laboratory of Neuroendocrinology, Rockefeller University (R.D.R., B.S.M.), New York, New York 10021; Department of Psychology, University of California (W.G.B.), Santa Barbara, California 93106; and Divisions of Reproductive Sciences and Neuroscience, Oregon National Primate Research Center (C.L.B.), Beaverton, Oregon 97006
Address all correspondence and requests for reprints to: Dr. Bruce S. McEwen, Laboratory of Neuroendocrinology, Rockefeller University, 1230 York Avenue, Box 165, New York, New York 10021. E-mail: mcewen{at}rockefeller.edu.
The role of estrogen (E) in promoting learning and memory in females has been well studied in both rodent and primate models. In female rats, E increases dendritic spine number, synaptogenesis, and synaptic proteins in the CA1 region of the hippocampus, an area of the brain that mediates learning and memory. In the present study, we used radioimmunocytochemistry to examine whether E and progesterone were capable of modulating the levels of pre- and postsynaptic proteins in the CA1 region of the female nonhuman primate hippocampus. It was found that E increased syntaxin, synaptophysin (presynaptic), and spinophilin (postsynaptic) levels in the stratum oriens and radiatum of the CA1 region, whereas combined E and progesterone treatment decreased these synaptic proteins to the levels found in untreated, spayed controls. Furthermore, progesterone treatment alone significantly increased synaptophysin levels in the stratum oriens and radiatum of the CA1 region. The levels of these synaptic proteins were unaltered by hormone treatment in the dentate gyrus, suggesting that this steroid-induced plasticity is hippocampal region specific. As these synaptic proteins are important components of the synaptic apparatus and reliable markers of synaptogenesis, it appears that E-induced increases in cognitive function of higher order mammals may be mediated in part by the effect of E on hippocampal synaptogenesis and synaptic plasticity.
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