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      Wired on Steroids: Sexual Differentiation of the Brain and Its Role in the Expression of Sexual Partner Preferences

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          Abstract

          The preference to seek out a sexual partner of the opposite sex is robust and ensures reproduction and survival of the species. Development of female-directed partner preference in the male is dependent on exposure of the developing brain to gonadal steroids synthesized during critical periods of sexual differentiation of the central nervous system. In the absence of androgen exposure, a male-directed partner preference develops. The development and expression of sexual partner preference has been extensively studied in rat, ferret, and sheep model systems. From these models it is clear that gonadal testosterone, often through estrogenic metabolites, cause both masculinization and defeminization of behavior during critical periods of brain development. Changes in the steroid environment during these critical periods result in atypical sexual partner preference. In this manuscript, we review the major findings which support the hypothesis that the organizational actions of sex steroids are responsible for sexual differentiation of sexual partner preferences in select non-human species. We also explore how this information has helped to frame our understanding of the biological influences on human sexual orientation and gender identity.

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          Most cited references 130

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          Polycystic Ovary Syndrome

          New England Journal of Medicine, 352(12), 1223-1236
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            Organizing action of prenatally administered testosterone propionate on the tissues mediating mating behavior in the female guinea pig.

             R Goy,  W YOUNG,  A A GERALL (1959)
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              Androgen production in women.

               Henry Burger (2002)
              To describe the sources, production rates, circulating concentrations, and regulatory mechanisms of the major androgen precursors and androgens in women. Review of the major published literature. Quantitatively, women secrete greater amounts of androgen than of estrogen. The major circulating steroids generally classified as androgens include dehydroepiandrosterone sulphate (DHEAS), dehydroepiandrosterone (DHEA), androstenedione (A), testosterone (T), and dihydrotestosterone in descending order of serum concentration, though only the latter two bind the androgen receptor. The other three steroids are better considered as pro-androgens. Dehydroepiandrosterone is primarily an adrenal product, regulated by adrenocorticotropic hormone (ACTH) and acting as a precursor for the peripheral synthesis of more potent androgens. Dehydroepiandrosterone is produced by both the ovary and adrenal, as well as being derived from circulating DHEAS. Androstenedione and testosterone are products of the ovary and the adrenal. Testosterone circulates both in its free form, and bound to protein including albumin and sex steroid hormone-binding globulin (SHBG), the levels of which are an important determinant of free testosterone concentration. The postmenopausal ovary is an androgen-secreting organ and the levels of testosterone are not directly influenced by the menopausal transition or the occurrence of menopause. Dihydrotestosterone (DHT) is primarily a peripheral product of testosterone metabolism. Severe androgen deficiency occurs in hypopituitarism, but other causes may lead to androgen deficiency, including Addison's disease, corticosteroid therapy, chronic illness, estrogen replacement (leads to elevated SHBG and, therefore, low free testosterone), premenopausal ovarian failure, or oophorectomy.
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                Author and article information

                Journal
                Front Endocrinol (Lausanne)
                Front Endocrinol (Lausanne)
                Front. Endocrin.
                Frontiers in Endocrinology
                Frontiers Research Foundation
                1664-2392
                14 August 2011
                03 October 2011
                2011
                : 2
                Affiliations
                1Department of Animal Science, University of Wyoming Laramie, WY, USA
                2Department of Zoology and Physiology, University of Wyoming Laramie, WY, USA
                3Department of Physiology and Pharmacology, Oregon Health and Science University Portland, OR, USA
                Author notes

                Edited by: Hubert Vaudry, University of Rouen, France

                Reviewed by: Micheal Baum, Boston University, USA; Robert James Handa, University of Arizona College of Medicine – Phoenix, USA

                *Correspondence: Charles E. Roselli, Department of Physiology and Pharmacology L334, Oregon Health and Science University, 3181 Sam Jackson Park Road, Portland, OR 97201-3098, USA. e-mail: rosellic@ 123456ohsu.edu

                This article was submitted to Frontiers in Neuroendocrine Science, a specialty of Frontiers in Endocrinology.

                Article
                10.3389/fendo.2011.00042
                3356085
                22654808
                Copyright © 2011 Alexander, Skinner and Roselli.

                This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.

                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 137, Pages: 11, Words: 11369
                Categories
                Endocrinology
                Review Article

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