Search Results

This chapter utilizes conspecific, offensive aggression in males and females as model systems to exemplify androgenic influences on aggressive behavior. This form of aggression is a productive behavior exhibited between same-sex conspecifics; its effects are reflected in dominance status and access to resources.

This chapter discusses the actions of gonadal hormones on synaptic plasticity and cellular replacement, and the potential mechanisms involved in the hormonal actions. It begins by examining the actions of ovarian hormones—estradiol and progesterone— on neural plasticity, followed by an analysis of the effects of testicular androgens. The neuroplastic effects of the adrenal androgen dehydroepiandrosterone (DHEA) are also considered when analyzing the effects of testicular androgens.

In a concomitant study, using electron microscopic stereological calculation, Woolley and McEwen (Woolley & McEwen, 1992) have demonstrated that, even during the ovarian cycle there is a fluctuation in the density of spine synapses in the stratum radiatum of the CA1 hippocampal subfield. Recent studies have also demonstrated that administration of male hormones to both gonadectomized male and female animals has the same synaptoplastic effects in the hippocampus as estrogen in females. However, there are major sex differences in the effectiveness and mechanisms of actions of the gonadal hormones, between males and females. This chapter reviews these differences to indicate where areas of uncertainty still remain, and suggests possible future avenues of research to explore the underlying mechanisms and potential neurological significance of these morphological responses to gonadal steroid exposure. Because the majority of the work in this field to date has focused on the CA1 area of the hippocampus, the chapter also focuses on sex differences in CA1 responses to androgen and estrogen.

Since prostate cancer began to attract more epidemiologic interest in the 1980s, numerous etiologic clues have been identified, and areas are now emerging as promising in the search for causes of prostate cancer. Besides genetic studies, exposures belonging to the broad categories of nutritional and hormonal factors are now being intensively investigated by epidemiologists. These areas are not mutually exclusive since dietary factors may act via hormonal pathways. Among nutritional factors, a protective effect of lycopene, selenium, vitamin E, and perhaps phytoestrogens and fish oil appear particularly promising, although no definite answers have yet emerged. Hormonal influences are also biologically plausible. While studies of steroid hormones, chiefly androgens, have not produced consistent results, a positive association between serum levels of IGF-1 and prostate cancer appears convincing.

Hormones have been proposed as internal signals that mediate life history trade-offs in both invertebrates and vertebrates. This chapter reviews the evidence for such a role. It outlines possible endocrine pathways by which such hormones could mediate life history trade-offs, focusing on sex steroids in vertebrates, and discusses evolutionary scenarios that may account for interspecific variation in hormonally regulated life-history trade-offs. Throughout, it attempts to outline future research directions.

The mammalian brain produces low levels of estrogens relative to the ovary and placenta, but by restricting synthesis to the site of estrogen action is able to exert powerful effects on neural development and function. The final step in estrogen production is the conversion of androgens to estrogens by cytochrome P450 aromatase. Recent evidence that hippocampus is capable of synthesizing estrogen de novo from cholesterol suggests a new paradigm for mammals in which sex steroids act independently of the gonads to regulate brain functions. In general, aromatase exhibits a dynamic and complex regulation that varies regionally, as well as with an animal’s age, sex, and physiologic status. This chapter summaries our current understanding of the distribution and regulation of aromatase in the mammalian brain and describes classic as well as novel functions for local estrogen synthesis in the brain.

Brain aromatase in fish is an exciting research topic because of several unconventional features that challenge the established view based on studies in other vertebrates. First, the brain of teleost fish exhibits a high degree of aromatase activity, especially in sexually mature animals. Given the emerging roles of estrogens in neurogenesis, the unique features of the adult fish brain suggest that, in addition to classical functions on brain sexual differentiation and sexual behavior, aromatase expression in radial glial cells could be involved in the modulation of the high proliferative activity in the brain of fish.

In the 1970s Carlos Beyers and his colleagues demonstrated that androgens that cannot be aromatized to estrogen also do not mimic testosterone in some test situations. These early tests of the “aromatization” hypothesis led to three sets of predictions to test the hypothesis: (1) If estrogen metabolites of testosterone are necessary for it to facilitate sexual behavior, then androgens that are not aromatized to estradiol will not sustain male or female sexual behavior. (2) If estrogen metabolites of testosterone are necessary to facilitate sexual behavior, then antiestrogen compounds should block testosterone facilitation of sexual behavior. (3) If estrogen metabolites of testosterone are required for facilitation of sexual behavior, compounds that inhibit the aromatase enzyme should block testosterone facilitation of sexual behavior. These three predictions directed much of the research on this topic for nearly two decades and led to increasingly better controlled experiments.

If we are to understand how hormone-mediated traits evolve, we need to examine the mechanisms underlying individual and sex differences in hormones and their effect on physiology, behavior, and ultimately fitness. This chapter begins to unravel this mechanistic black box, focusing on individual and sex variation in production of testosterone (T), sensitivity to T, and the downstream effects of T on organismal biological processes, employing the dark-eyed junco as a model. Correlational and experimental studies at each of these levels of analysis reveal a remarkable degree of independence among the constituent parts of the endocrine system. Further, although the sexes show striking similarities in the abundance of transcript for sex steroid binding and processing molecules at neural targets, the downstream genomic effects of hormones differ between males and females. Thus, while hormonal pleiotropy produces suites of correlated traits, individual variation in circulating T, sensitivity to T, and T-mediated gene expression exists along many different axes within the endocrine system, providing a multitude of different mechanisms on which selection could act. Likewise, the sexes appear to have found partial solutions to sexual conflict over T at each of these parts of the endocrine system, particularly with respect to the downstream genomic effects of T.

This chapter explores the maternal effects on offspring personality development in both oviparous and placental vertebrates. In particular, it discusses how prenatal maternal stress and prenatal exposure to varying levels of androgens and estrogens can result in stable individual differences in offspring physiology and behavior later in life.

Although the potent estrogen, 17β‎-estradiol (E2), has long been known to regulate the hippocampal dendritic spine density and synaptic plasticity, the molecular mechanisms through which it does so are less well understood. This chapter discusses the rapid modulation of hippocampal dendritic spine density and synaptic plasticity in male and female rats, with particular attention to studies in hippocampal slices from male rats. Among the mechanisms described are the roles of specific cell-signaling kinases and estrogen receptors in mediating the effects of E2 and progesterone on hippocampal neurons. In addition, dynamic changes of spine structures over time and sex differences in spine regulation are also considered. Finally, the chapter ends by discussing the importance of local hippocampal synthesis of E2 and androgens to hippocampal spine morphology and plasticity.

Prostate cancer is the most common solid tumor and the second leading cause of cancer-related mortality in American men. Worldwide, prostate cancer ranks second and fifth as a cause of cancer and cancer deaths, respectively. Despite the international burden of disease due to prostate cancer, its etiology is unclear in most cases. Established risk factors include age, race/ancestry, and family history of the disease. Prostate cancer has a strong heritable component, and genome-wide association studies have identified over 110 common risk-associated genetic variants. Family-based sequencing studies have also found rare mutations (e.g., HOXB13) that contribute to prostate cancer susceptibility. Numerous environmental and lifestyle factors (e.g., obesity, diet) have been examined in relation to prostate cancer incidence, but few modifiable exposures have been consistently associated with risk. Some of the variability in results may be related to etiological heterogeneity, with different causes underlying the development of distinct disease subgroups.

This chapter discusses the effect of hormones in the central nervous system or genitalia that influence the behaviour and sexual attractiveness of female primates. It explores the function of adrenal glands, as well as oestrogens, androgens, and progestagen in female sexuality. It explains the hypothalamic basis of sexual receptivity and proceptivity by giving a neural model of proceptivity in female primates. It also examines the neural substrates that govern sexual behaviour in females by comparing and contrasting the limited evidence on primates with more extensive information on the brain and sexual behaviour in rodents and other non-primate mammals.

This chapter discusses the seasonal changes in hormones and sexual behaviour of male primates. It examines the effects of castration, testosterone replacement, anti-androgens, and metabolites on male primates. Sexually experienced males castrated in adulthood rarely mount females and fail to intromit when observed six to twelve months after surgery. The chapter also explores the sources of individual variability in sexual behaviour such as individual differences in circulating androgen levels, the role of previous sexual experience and the role of the female partner. It addresses the difference between the peripheral and central effects of androgens upon male sexuality; and discusses the factors that impinge hypothalamic mechanisms.

This chapter describes the role of early testosterone exposure in gender development. It discusses these hormonal influences and how they relate to genetic influences, socialization by others, and self-socialization, in shaping gender development. To illustrate these influences, it focuses primarily on childhood play behavior. This focus is used because childhood play behavior shows large differences between the sex categories boy and girl to which children are assigned at birth. Also, childhood play behavior has been studied extensively, providing perhaps the best example of how a gender-related behavior can be influenced by a range of factors at levels of organization from the cellular to the societal working in concert over time.

The neuroendocrine system is the interface between the endocrine and nervous systems. This chapter presents an overview of the neuroendocrine system and endogenous hormones, with a primary focus on the hypothalamic-pituitary-gonadal (HPG) axis, the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-thyroid axis (HPT). The importance of impacts of exogenous compounds, both natural and man-made, on the neuroendocrine system is discussed, with a focus on endocrine-disruptive actions of plant-derived phytoestrogens and the role of the aryl hydrocarbon receptor as an environmental sensor. The impacts of EDCs on feed-forward and negative feedback regulation of neuroendocrine functions, including those mediated by estrogen, androgen, and thyroid pathways, as well as other less studied pathways of hormonal signaling that involve disruption of neurosteroids, peptide hormones, and adrenal hormone signaling are also presented.