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The Journal of Neuroscience, March 1, 2006, 26(9):2571-2578; doi:10.1523/JNEUROSCI.3440-05.2006

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Development/Plasticity/Repair
Estrogen Alters Spine Number and Morphology in Prefrontal Cortex of Aged Female Rhesus Monkeys

Jiandong Hao,¹ Peter R. Rapp,^1,2 Abba E. Leffler,¹ Shoshana R. Leffler,¹ William G. M. Janssen,¹ Wendy Lou,⁶ Heather McKay,⁵ Jeffrey A. Roberts,⁷ Susan L. Wearne,^1,3,4 Patrick R. Hof,^1,2,4 and John H. Morrison^1,2,4

¹Fishberg Department of Neuroscience and Kastor Neurobiology of Aging Laboratories, ²Department of Geriatrics and Adult Development, ³Center for Biomathematical Sciences, ⁴Computational Neurobiology and Imaging Center, Mount Sinai School of Medicine, New York, New York 10029, ⁵California National Primate Research Center, University of California, Davis, California 95616, ⁶Department of Public Health Sciences, University of Toronto, Toronto, Ontario, Canada M5T 3M7, and ⁷Valley Biosystems, West Sacramento, California 95605

Correspondence should be addressed to Dr. John H. Morrison, Department of Neuroscience, Box 1065, Mount Sinai School of Medicine, New York, NY 10029. Email: John.Morrison{at}mssm.edu

Long-term cyclic treatment with 17-estradiol reverses age-related impairment in ovariectomized rhesus monkeys on a test of cognitive function mediated by the prefrontal cortex (PFC). Here, we examined potential neurobiological substrates of this effect using intracellular loading and morphometric analyses to test the possibility that the cognitive benefits of hormone treatment are associated with structural plasticity in layer III pyramidal cells in PFC area 46. 17-Estradiol did not affect several parameters such as total dendritic length and branching. In contrast, 17-estradiol administration increased apical and basal dendritic spine density, and induced a shift toward smaller spines, a response linked to increased spine motility, NMDA receptor-mediated activity, and learning. These results document that, although the aged primate PFC is vulnerable in the absence of factors such as circulating estrogens, it remains responsive to long-term cyclic 17-estradiol treatment, and that increased dendritic spine density and altered spine morphology may contribute to the cognitive benefits of such treatment.

Key words: plasticity; neocortex; estradiol; hormone; cognition; pyramidal cell

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Received Aug. 15, 2005; revised Jan. 20, 2006; accepted Jan. 21, 2006.

Correspondence should be addressed to Dr. John H. Morrison, Department of Neuroscience, Box 1065, Mount Sinai School of Medicine, New York, NY 10029. Email: John.Morrison{at}mssm.edu

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