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Gonadal Hormones (gonadal + hormones)
Selected AbstractsThe Influence of Gonadal Hormones on Neuronal Excitability, Seizures, and Epilepsy in the FemaleEPILEPSIA, Issue 9 2006Helen E. Scharfman Summary:, It is clear from both clinical observations of women, and research in laboratory animals, that gonadal hormones exert a profound influence on neuronal excitability, seizures, and epilepsy. These studies have led to a focus on two of the primary ovarian steroid hormones, estrogen and progesterone, to clarify how gonadal hormones influence seizures in women with epilepsy. The prevailing view is that estrogen is proconvulsant, whereas progesterone is anticonvulsant. However, estrogen and progesterone may not be the only reproductive hormones to consider in evaluating excitability, seizures, or epilepsy in the female. It seems unlikely that estrogen and progesterone would exert single, uniform actions given our current understanding of their complex pharmacological and physiological relationships. Their modulatory effects are likely to depend on endocrine state, relative concentration, metabolism, and many other factors. Despite the challenges these issues raise to future research, some recent advances have helped clarify past confusion in the literature. In addition, testable hypotheses have developed for complex clinical problems such as "catamenial epilepsy." Clinical and animal research, designed with the relevant endocrinological and neurobiological issues in mind, will help advance this field in the future. [source] Gonadal hormone modulation of hippocampal neurogenesis in the adultHIPPOCAMPUS, Issue 3 2006Liisa A.M. Galea Abstract Gonadal hormones modulate neurogenesis in the dentate gyrus (DG) of adult rodents in complex ways. Estradiol, the most potent estrogen, initially enhances and subsequently suppresses cell proliferation in the dentate gryus of adult female rodents. Much less is known about how estradiol modulates neurogenesis in the adult male rodent; however, recent evidence suggests that estradiol may have a moderate effect on cell proliferation but enhances cell survival in the DG of newly synthesized cells but only when estradiol is administered during a specific stage in the cell maturation cycle in the adult male rodent. Testosterone likely plays a role in adult neurogenesis, although there have been no direct studies to address this. However, pilot studies from our laboratory suggest that testosterone up-regulates cell survival but not cell proliferation in the DG of adult male rats. Progesterone appears to attenuate the estradiol-induced enhancement of cell proliferation. Neurosteroids such as allopregnalone decrease neurogenesis in adult rodents, while pregnancy and motherhood differentially regulate adult neurogenesis in the adult female rodent. Very few studies have investigated the effects of gonadal hormones on male rodents; however, studies have indicated that there is a gender difference in the response to hormone-regulated hippocampal neurogenesis in the adult. Clearly, more work needs to be done to elucidate the effects of gonadal hormones on neurogenesis in the DG of both male and female rodents. © 2006 Wiley-Liss Inc. [source] Foster mother care but not prenatal morphine exposure enhances cocaine self-administration in young adult male and female ratsDEVELOPMENTAL PSYCHOBIOLOGY, Issue 5 2007I. Vathy Abstract The present study was designed to investigate cocaine self-administration in adult male and female rats exposed prenatally to morphine. Pregnant dams were injected two times a day with either saline, analgesic doses of morphine or no drug at all (controls) on gestation Days 11,18. One day after birth, litters were cross-fostered such that control dams were paired with one another and their litters were crossed; saline- and morphine-treated dams were paired and half of each saline litter was crossed with half of each morphine litter. Thus, each mother (control, saline, and morphine) raised half of her own and half of the adopted litter. At the age of 60 days, males and females were trained first to lever press for sucrose pellets and then for cocaine. Once the lever-pressing behavior was learned and baseline level of this activity was established, animals received a cocaine (.5 mg/kg per infusion) reward for each correct response on the active lever during the next 9-day session. The data demonstrate that adult control, saline- and morphine-exposed male rats self-administer cocaine at a similar rate independent of their prenatal treatment. Adult female rats self-administer cocaine at a higher rate than male rats. Further, saline- and morphine-exposed females in diestrus self-administer more than females in proestrus phase of the estrous cycle, while control females show no such differences. In addition, fostering induces increase in cocaine self-administration in all groups of male rats regardless of prenatal drug exposure. In females, the only fostering-induced increase is in prenatally saline-exposed female rats raised by morphine-treated foster mother. Thus, our results suggest that the prenatal drug exposure does not induce changes in lever-pressing behavior for cocaine reward in adult male and female rats, but it sensitizes the animals to postnatal stimuli such as gonadal hormones and/or rearing conditions that result in increased drug self-administration. © 2007 Wiley Periodicals, Inc. Dev Psychobiol 49: 463-473, 2007. [source] The Influence of Gonadal Hormones on Neuronal Excitability, Seizures, and Epilepsy in the FemaleEPILEPSIA, Issue 9 2006Helen E. Scharfman Summary:, It is clear from both clinical observations of women, and research in laboratory animals, that gonadal hormones exert a profound influence on neuronal excitability, seizures, and epilepsy. These studies have led to a focus on two of the primary ovarian steroid hormones, estrogen and progesterone, to clarify how gonadal hormones influence seizures in women with epilepsy. The prevailing view is that estrogen is proconvulsant, whereas progesterone is anticonvulsant. However, estrogen and progesterone may not be the only reproductive hormones to consider in evaluating excitability, seizures, or epilepsy in the female. It seems unlikely that estrogen and progesterone would exert single, uniform actions given our current understanding of their complex pharmacological and physiological relationships. Their modulatory effects are likely to depend on endocrine state, relative concentration, metabolism, and many other factors. Despite the challenges these issues raise to future research, some recent advances have helped clarify past confusion in the literature. In addition, testable hypotheses have developed for complex clinical problems such as "catamenial epilepsy." Clinical and animal research, designed with the relevant endocrinological and neurobiological issues in mind, will help advance this field in the future. [source] X chromosome number causes sex differences in gene expression in adult mouse striatumEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2009Xuqi Chen Abstract Previous research suggests that sex differences in the nigrostriatal system are created by direct effects of the sex chromosomes (XX vs. XY), independent of the action of gonadal hormones. Here we tested for sex chromosome effects on expression of three mRNAs in the striatum and nucleus accumbens of adult mice of the four core genotypes model (XX and XY gonadal males, XX and XY gonadal females). Mice were gonadectomized (GDX) at 47,51 days old to eliminate group differences in the levels of gonadal steroids. Three weeks later, mice were killed and brains collected for in situ hybridization of the striatum, or the striatum was dissected out for quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). Expression in XX and XY mice was measured by in situ hybridization using riboprobes encoding the dynorphin precursor Pdyn (prodynorphin), the substance P precursor Tac1 (preprotachykinin) or dopamine D2 receptor. XX mice had higher expression, relative to XY mice of the same gonadal sex, of Pdyn and Tac1 mRNA in specific striatal regions. Quantitative PCR confirmed that GDX XX mice have higher Pdyn expression in striatum than XY mice, regardless of their gonadal sex. XX had higher Pdyn expression than XY or XO mice, indicating that the sex chromosome effect is the result of XX vs. XY differences in the number of X chromosomes, probably because of sex differences in the expression of X gene(s) that escape inactivation. We detected no sex chromosome effect on D2 receptor mRNA. [source] Test of Nyborg's General Trait Covariance (GTC) model for hormonally guided development by means of structural equation modelingEUROPEAN JOURNAL OF PERSONALITY, Issue 3 2003Martin Reuter Nyborg's General Trait Covariance (GTC) model for hormonally guided development investigates the influence of gonadal hormones and fluid intelligence on body build, achievement, and socioeconomic variables. According to the model, testosterone should be negatively related to height, fat/muscle ratio, intelligence, income, and education. It is conceived that this influence should be determined to a great extent by mutual relationships between these variables. The model was tested by means of structural equation modeling (SEM) in a sample of 4375 males who had served in the United States Armed Forces. The results largely confirm Nyborg's androtype model but in addition reflect the relationships between the variables included in a quantitative causal manner. It could be shown that testosterone has a negative influence on crystallized intelligence and that this effect is mainly mediated by the negative influence of testosterone on education. An additional multiple group analysis testing for structural invariance across age groups revealed that the mediating role of education is more pronounced in old veterans. Copyright © 2002 John Wiley & Sons, Ltd. [source] Gonadal hormone modulation of hippocampal neurogenesis in the adultHIPPOCAMPUS, Issue 3 2006Liisa A.M. Galea Abstract Gonadal hormones modulate neurogenesis in the dentate gyrus (DG) of adult rodents in complex ways. Estradiol, the most potent estrogen, initially enhances and subsequently suppresses cell proliferation in the dentate gryus of adult female rodents. Much less is known about how estradiol modulates neurogenesis in the adult male rodent; however, recent evidence suggests that estradiol may have a moderate effect on cell proliferation but enhances cell survival in the DG of newly synthesized cells but only when estradiol is administered during a specific stage in the cell maturation cycle in the adult male rodent. Testosterone likely plays a role in adult neurogenesis, although there have been no direct studies to address this. However, pilot studies from our laboratory suggest that testosterone up-regulates cell survival but not cell proliferation in the DG of adult male rats. Progesterone appears to attenuate the estradiol-induced enhancement of cell proliferation. Neurosteroids such as allopregnalone decrease neurogenesis in adult rodents, while pregnancy and motherhood differentially regulate adult neurogenesis in the adult female rodent. Very few studies have investigated the effects of gonadal hormones on male rodents; however, studies have indicated that there is a gender difference in the response to hormone-regulated hippocampal neurogenesis in the adult. Clearly, more work needs to be done to elucidate the effects of gonadal hormones on neurogenesis in the DG of both male and female rodents. © 2006 Wiley-Liss Inc. [source] Leptin and varicocele-related spermatogenesis dysfunction: animal experiment and clinical studyINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 5 2009Bin Chen Summary The objective of this study was to explore the relationships between varicocele-related spermatogenesis dysfunction and the expression of leptin and leptin receptors. In rats with experimental varicocele, the function of spermatogenesis, the expression of leptin and leptin receptors in testes were analysed; and in patients with varicocele-related male infertility, serum and seminal plasma levels of leptin, gonadal hormones and semen parameters were evaluated. In the testes of rats, leptin was expressed in seminiferous tubules and intersitium, leptin receptor was predominantly expressed in interstitium. The expression of leptin and its receptor in the testis of rats was not related to the weight of rat, but was inversely related to the weight of testis (r = ,0.408, p = 0.009 and r = ,0.433, p = 0.005, respectively), the Johnsen scores (r = ,0.916, p = 0.000 and r = ,0.863, p = 0.000, respectively), the seminiferous tubules diameter (r = ,0.853, p = 0.000 and r = ,0.870, p = 0.000, respectively) and the thickness of seminiferous epithelium (r = ,0.929, p = 0.000 and r = ,0.948, p = 0.000, respectively). In varicocele patients (N = 40), the sperm concentration and motility were significantly lower (p = 0.000) than those in the control group (N = 25), and the leptin level in seminal plasma was significantly higher (p = 0.000) than that in the control group. The leptin in serum and seminal plasma was positively related (r = 0.223, p = 0.002). The seminal plasma leptin level was inversely related to sperm concentration (r = ,0.632, p = 0.000) and motility (r = ,0.635, p = 0.000). There was no significant relation between serum leptin and seminal parameters and between leptin and gonadal hormone values. The dysfunction of spermatogenesis in varicocele-related infertile male is associated with increase in leptin and leptin receptors. Leptin may have local effects on the function of testis and spermatogenesis. [source] The physiological basis of human sexual arousal: neuroendocrine sexual asymmetryINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 2 2005ION G. MOTOFEI Summary Normal sexual arousal and response suppose an integrated process involving both physiological and psychological processes. However, the current understanding of sexual arousal does not provide a coherent model that accounts for the integration of multiple physiological systems that subsequently generate a coordinated sexual response at both the spinal peripheral and cerebral central levels. Herein we suggest a model that involves both sympathetic and parasympathetic activation during sexual arousal via the two classes of gonadal hormones, androgens and oestrogens. We discuss the manner in which gonadal hormones may activate such a system, transforming pre-pubertal (non-erotic) genital stimulation to post-pubertal erogenization of stimulation and subsequent sexual arousal. Finally, we indicate that the different balance of androgens and oestrogens in men and women may generate asymmetric effects on each of the components of the autonomic nervous system, thereby explaining some of the differences in patterns of sexual arousal and the responses cycle across the sexes. [source] Leptin, body composition, adrenal and gonadal hormones among captive male baboonsJOURNAL OF MEDICAL PRIMATOLOGY, Issue 6 2003M.P. Muehlenbein Abstract:, Morphometric and hormonal measures were collected from 21 captive savanna baboons (Papio cynocephalus) maintained at the Tulane National Primate Research Center in order to determine age-related patterns in leptin levels over the life course as well as their relationships to body composition and adrenal and gonadal steroids. Comparison of leptin levels between peri-pubertal, adolescent, young adult, and fully mature males show lower levels among adolescent as compared with young adult males (P = 0.05 by Kruskal,Wallis ANOVA). In addition, abdominal fat varied among age groups (P = 0.003 by Kruskal,Wallis ANOVA) with the peri-pubertal animals lower than the adolescents, young adults, and prime adults. However leptin was not related to any measure of body composition, including abdominal fat, or to adrenal hormones (dehydroepiandrosterone, dehydroepiandrosterone-sulfate, and cortisol) or gonadal hormones (testosterone and estradiol). Age-related changes in leptin appear similar to those reported for captive rhesus macaques, while the failure to find an association between leptin and abdominal fat is interestingly different. These results confirm elevated levels of leptin in captive baboons compared with their wild counterparts and suggest that they result from changes in fetal development. [source] Examining the Intersection of Sex and Stress in Modelling Neuropsychiatric DisordersJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2009N. Goel Sex-biased neuropsychiatric disorders, including major depressive disorder and schizophrenia, are the major cause of disability in the developed world. Elevated stress sensitivity has been proposed as a key underlying factor in disease onset. Sex differences in stress sensitivity are associated with corticotrophin-releasing factor (CRF) and serotonin neurotransmission, which are important central regulators of mood and coping responses. To elucidate the underlying neurobiology of stress-related disease predisposition, it is critical to develop appropriate animal models of stress pathway dysregulation. Furthermore, the inclusion of sex difference comparisons in stress responsive behaviours, physiology and central stress pathway maturation in these models is essential. Recent studies by our laboratory and others have begun to investigate the intersection of stress and sex where the development of mouse models of stress pathway dysregulation via prenatal stress experience or early-life manipulations has provided insight into points of developmental vulnerability. In addition, examination of the maturation of these pathways, including the functional importance of the organisational and activational effects of gonadal hormones on stress responsivity, is essential for determination of when sex differences in stress sensitivity may begin. In such studies, we have detected distinct sex differences in stress coping strategies where activational effects of testosterone produced females that displayed male-like strategies in tests of passive coping, but were similar to females in tests of active coping. In a second model of elevated stress sensitivity, male mice experiencing prenatal stress early in gestation showed feminised physiological and behavioural stress responses, and were highly sensitive to a low dose of selective serotonin reuptake inhibitors. Analyses of expression and epigenetic patterns revealed changes in CRF and glucocorticoid receptor genes in these mice. Mechanistically, stress early in pregnancy produced a significant sex-dependent effect on placental gene expression that was supportive of altered foetal transport of key growth factors and nutrients. These mouse models examining alterations and hormonal effects on development of stress pathways provide necessary insight into how specific stress responses can be reprogrammed early in development resulting in sex differences in stress sensitivity and neuropsychiatric disease vulnerability. [source] Effects of Prenatal Ethanol Exposure on Hypothalamic-Pituitary-Adrenal Function Across the Estrous CycleALCOHOLISM, Issue 6 2009Ni Lan Background:, Rats prenatally exposed to ethanol (E) typically show increased hypothalamic-pituitary-adrenal (HPA) responses to stressors in adulthood. Importantly, prenatal ethanol may differentially alter stress responsiveness in male and female offspring, suggesting a role for the gonadal hormones in mediating the effects of ethanol on HPA activity. We investigated the role of ethanol-induced changes in hypothalamic-pituitary-gonadal (HPG) activity in the differential HPA regulation observed in E compared to control females across the estrous cycle. Methods:, Peripheral hormones and changes in central neuropeptide mRNA levels were measured across the estrous cycle in adult female offspring from E, pair-fed (PF) and ad libitum-fed control (C) dams. Results:, Ethanol females showed normal estrous cyclicity (vaginal smears) but delayed sexual maturation (vaginal opening). Both HPG and HPA activity were differentially altered in E (and in some cases, PF) compared to control females as a function of estrous cycle stage. In relation to HPG activity, E and PF females had higher basal and stress estradiol (E2) levels in proestrus compared to other phases of the cycle, and decreased GnRH mRNA levels compared to C females in diestrus. Further, E females had greater variation in LH than PF and C females across the cycle, and in proestrus, only E females showed a significant LH increase following stress. In relation to HPA activity, both basal and stress CORT levels and overall ACTH levels were greater in E than in C females in proestrus. Furthermore, AVP mRNA levels were increased overall in E compared to PF and C females. Conclusions:, These data demonstrate ethanol-induced changes in both HPG and HPA activity that are estrous phase-specific, and support the possibility that changes in HPA activity in E females may reflect differential sensitivity to ovarian steroids. E females appear to have an increased HPA sensitivity to E2, and a possible shift toward AVP regulation of HPA activity. That PF were similar to E females on some measures suggests that nutritional effects of diet or food restriction played a role in mediating at least some of the changes observed. [source] Gender-related changes in the avian vasotocin system during ontogenyMICROSCOPY RESEARCH AND TECHNIQUE, Issue 1 2001Aleksandr Jurkevich Abstract The arginine vasotocin (AVT) system of the avian brain includes a sexually dimorphic part that extends from the caudal part of preoptic region through the medial part of the bed nucleus of stria terminalis (BSTm) to the lateral septum. It is composed of the parvocellular neurons located in the BSTm and the dense innervation of the medial preoptic region and lateral septum. In this part of the brain, AVT expression is stronger in males than in females in a few bird species investigated to date. This review focuses on the ontogeny of sexual differences in the vasotocinergic system of two gallinaceous species, domestic chicken and Japanese quail, and on the role of gonadal hormones in organizing during development and maintaining in adulthood these differences. Parvocellular AVT neurons become discernible in the BSTm of males and females during the second half of embryonic development. These cells undergo a profound and irreversible sexual differentiation during ontogenetic development. Recent findings demonstrate a dual role of estrogens in the organization and activation of sex differences in the AVT system. During the embryonic period of ontogeny, estrogens differentiate the AVT system in a sexually dimorphic manner in parallel with the differentiation of sexual behavior, while in adulthood estrogens, locally produced from testosterone in the male brain, activate AVT synthesis in the BSTm. The sexually dimorphic part of the AVT system is sensitive to a number of abiotic factors such as light, temperature, and water availability. It is suggested that sex dimorphic vasotocinergic systems could be implicated in processes of social recognition in various behavioral contexts. Microsc. Res. Tech. 55:27,36, 2001. © 2001 Wiley-Liss, Inc. [source] Distribution of sex steroid hormone receptors in the brain of an African cichlid fish, Astatotilapia burtoniTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 16 2010Lauren A. Munchrath Abstract Sex steroid hormones released from the gonads play an important role in mediating social behavior across all vertebrates. Many effects of these gonadal hormones are mediated by nuclear steroid hormone receptors, which are crucial for integration in the brain of external (e.g., social) signals with internal physiological cues to produce an appropriate behavioral output. The African cichlid fish Astatotilapia burtoni presents an attractive model system for the study of how internal cues and external social signals are integrated in the brain as males display robust plasticity in the form of two distinct, yet reversible, behavioral and physiological phenotypes depending on the social environment. In order to better understand where sex steroid hormones act to regulate social behavior in this species, we have determined the distribution of the androgen receptor, estrogen receptor alpha, estrogen receptor beta, and progesterone receptor mRNA and protein throughout the telencephalon and diencephalon and some mesencephalic structures of A. burtoni. All steroid hormone receptors were found in key brain regions known to modulate social behavior in other vertebrates including the proposed teleost homologs of the mammalian amygdalar complex, hippocampus, striatum, preoptic area, anterior hypothalamus, ventromedial hypothalamus, and ventral tegmental area. Overall, there is high concordance of mRNA and protein labeling. Our results significantly extend our understanding of sex steroid pathways in the cichlid brain and support the important role of nuclear sex steroid hormone receptors in modulating social behaviors in teleosts and across vertebrates. J. Comp. Neurol. 518:3302,3326, 2010. © 2010 Wiley-Liss, Inc. [source] Sex differences in stress responses to transportation in goats: Effects of gonadal hormonesANIMAL SCIENCE JOURNAL, Issue 6 2003Masato AOYAMA ABSTRACT The present study examined sex differences and the involvement of gonadal hormones in stress responses caused by road transportation in Shiba goats. In experiment 1, we investigated the stress responses of males and females to transportation. Plasma levels of cortisol (Cor) significantly increased during 1 h of transportation, and those in females were significantly higher than those in males. Plasma glucose (Glu) and free fatty acid (FFA) levels also increased similarly in both females and males by transportation, and there were no sex differences. Food intake following transportation decreased only in males compared with that in the basal session, in which the animals were not transported. Experiment 2 examined the involvement of gonadal hormones in stress responses to transportation using castrated males. Goats were given cholesterol (Cho), 5,-dihydrotestosterone (DHT) or 17,-estradiol (Es). The plasma Cor levels increased during transportation regardless of hormone treatment, and those in DHT treated goats were significantly lower than those in Cho or Es treated animals. Plasma Glu and FFA levels also increased during transportation, regardless of hormone treatment, and there were no differences between treatments. Food intake following transportation was significantly lower than that in the basal session only in goats given DHT. In conclusion, gender affects Cor secretion that is increased by transportation and the decrease of food intake following transportation in Shiba goats, and the major cause of these differences is androgen. [source] Expression of proopiomelanocortin and proenkephalin mRNA in sexually dimorphic brain regions are altered in adult male and female rats treated prenatally with morphineCHEMICAL BIOLOGY & DRUG DESIGN, Issue 5 2004lamberová Abstract:, The present study demonstrates that prenatal morphine exposure on gestation days 11,18 differentially alters proopiomelanocortin (POMC) and proenkephalin (pENK) mRNA in the hypothalamus and limbic system of adult male and female rats. In adult, prenatally morphine-exposed male rats POMC mRNA levels are decreased in the arcuate nucleus of the hypothalamus (ARC), while the pENK mRNA levels are increased in the paraventricular nucleus of the hypothalamus (PVN) and in the ventrolateral subdivision of the ventromedial nucleus of the hypothalamus (VMH), specifically in the ventrolateral subdivision of the VMH. In adult, prenatally morphine-exposed female rats, POMC mRNA levels in the ARC are increased in ovariectomized (OVX) but not in OVX, estradiol benzoate- (EB) or EB- and progesterone- (P) treated females. In contrast, pENK mRNA levels are decreased in the VMH of morphine-exposed, OVX females and increased in EB-treated females. Further, prenatal morphine exposure decreases pENK mRNA in the ARC and increases it in the medial pre-optic area independently of female gonadal hormones. Finally, POMC mRNA levels are increased in the ARC of saline-exposed, EB- or EB- and P-treated females but not in OVX females. Thus, the present study suggests that prenatal morphine exposure sex and brain region specifically alters the level of POMC and pENK mRNA. [source] | |||||||||||||