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Submitted on September 19, 2003
Accepted on November 17, 2003
1 Departments of Obstetrics and Gynecologyand Neurobiology, Yale University School of Medicine, New Haven CT 06520; Laboratory of Molecular Neurobiology, Biological Research Center, Hungarian Academy of Sciences, H-6726 Szeged, Hungary; and Center for Reproductive Sciences, Columbia University Medical School, New York NY 10032.
* To whom correspondence should be addressed. E-mail: csaba.leranth{at}yale.edu.
This study tests the hypothesis that dehydroepiandrosterone (DHEA) stimulates formation of hippocampal CA1 spine synapses in ovariectomized (OVX) rats. Subcutaneous injections of DHEA (1 mg/day for two days) increased CA1 spine synapse density by more than 50% compared with vehicle-injected animals. The effect of DHEA on CA1 synapse density was abolished by pretreatment with the non-steroidal aromatase inhibitor, letrozole. DHEA treatment, with or without letrozole, had no detectable uterotrophic effect. These observations are consistent with the hypothesis that DHEA treatment may be capable of reversing the decline in hippocampal spine synapse density observed following loss of ovarian steroid hormone secretion. The blockade of the synaptic response to DHEA by letrozole, despite the lack of a uterotrophic response to this steroid, suggests that the hippocampal response to DHEA may be mediated via aromatization in the brain.
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