Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 104, Issue 27, Pages 11465-11470Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0704757104
Keywords
aging estradiol; hormone; neocortex; plasticity
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Funding
- NCRR NIH HHS [RR16754] Funding Source: Medline
- NIA NIH HHS [P01 AG016765, AG06647, R37 AG010606, R37 AG006647, AG10606, R01 AG006647, R01 AG010606, AG16765] Funding Source: Medline
- NIMH NIH HHS [MH60734, R01 MH060734, MH58911, P50 MH058911] Funding Source: Medline
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We previously reported that long-term cyclic estrogen (E) treatment reverses age-related impairment of cognitive function mediated by the clorsolateral prefrontal cortex (cdIPFC) in ovariectomized (OVX) female rhesus monkeys, and that E induces a corresponding increase in spine density in layer III dPFC pyramidal neurons. We have now investigated the effects of the same E treatment in young adult females. In contrast to the results for aged monkeys, E treatment failed to enhance dIPFC-dependent task performance relative to vehicle control values (group young OVX+Veh) but nonetheless led to a robust increase in spine density. This response was accompanied by a decline in dendritic length, however, such that the total number of spines per neuron was equivalent in young OVX+Veh and OVX+E groups. Robust effects of chronological age, independent of ovarian hormone status, were also observed, comprising significant age-related declines in dendritic length and spine density, with a preferential decrease in small spines in the aged groups. Notably, the spine effects were partially reversed by cyclic E administration, although young OVX+Veh monkeys still had a higher complement of small spines than did aged E treated monkeys. In summary, layer III pyramidal neurons in the dPFC are sensitive to ovarian hormone status in both young and aged monkeys, but these effects are not entirely equivalent across age groups. The results also suggest that the cognitive benefit of E treatment in aged monkeys is mediated by enabling synaptic plasticity through a cyclical increase in small, highly plastic dendritic spines in the primate dIPFC.
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