Home About us Contact
|
Home About us Contact | ||
|
|
||
Hormone Surge (hormone + surge)
Selected AbstractsKisspeptin and the Preovulatory Gonadotrophin-Releasing Hormone/Luteinising Hormone Surge in the Ewe: Basic Aspects and Potential Applications in the Control of OvulationJOURNAL OF NEUROENDOCRINOLOGY, Issue 7 2010A. Caraty The identification of the neural mechanisms controlling ovulation in mammals has long been a ,holy grail' over recent decades, although the recent discovery of the kisspeptin systems has totally changed our views on this subject. Kisspeptin cells are the major link between gonadal steroids and gonadotrophin-releasing hormone (GnRH) neurones. In the female rodent, kisspeptin cells of the preoptic area are involved in the positive-feedback action of oestrogen on GnRH secretion, although the picture appears more complicated in the ewe. As in rodents, activation of preoptic kisspeptin neurones accompanies the GnRH surge in the ewe but an active role for arcuate kisspeptin neurones has also been proposed. Experimentally, kisspeptin is able to restore reproductive function when the hypothalamic-hypophyseal ovarian axis is quiescent. For example, i.v. infusion of a low dose of peptide in anoestrous ewes induces an immediate and sustained release of gonadotrophin, which subsides and then provokes a luteinising hormone (LH) surge a few hours later. This pharmacological intervention induces the same hormonal changes normally observed during the follicular phase of the oestrous cycle, including the secretion of oestrogen and its negative- and positive-feedback actions on the secretion of LH and follicle-stimulating hormone. Accordingly, a high percentage of kisspeptin-infused animals ovulated. Although the multiple facets of how the kisspeptin systems modulate GnRH secretion are not totally understood, the demonstration that exogenous kisspeptin administration can induce ovulation in anovulatory animals paves the way for future therapeutic applications aiming to control reproduction. [source] Elevated KiSS-1 Expression in the Arcuate Nucleus Prior to the Cyclic Preovulatory Gonadotrophin-Releasing Hormone/Lutenising Hormone Surge in the Ewe Suggests a Stimulatory Role for Kisspeptin in Oestrogen-Positive FeedbackJOURNAL OF NEUROENDOCRINOLOGY, Issue 10 2006K. M. Estrada Kisspeptins are encoded by the gene KiSS-1 and regulate gonadotrophin-releasing hormone (GnRH) and gonadotrophin secretion in various species, including humans. Here, we quantify gene expression of KiSS-1 in the arcuate nucleus (ARC) across the ovine oestrous cycle and demonstrate an increase in the caudal division of the ARC during the preovulatory period. These data strongly suggest that kisspeptins are involved in the generation of the preovulatory GnRH and luteinising hormone surge. [source] Alteration in Hypothalamic Neuropeptide Y (NPY) Secretion May Underlie Female Reproductive Ageing: Induction of Steroid-Induced Luteinising Hormone Surge by NPY in Ovariectomised Aged RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2006A. Sahu A large body of evidence suggests that a defect in the hypothalamic function may be the primary cause of reproductive ageing in female rats. We have previously shown that luteinising hormone (LH)-surge associated changes in hypothalamic neuropeptide Y (NPY) gene expression and median eminence (ME) NPY levels seen in young rats do not occur in middle-aged (MA) rats. The present study examined whether hypothalamic NPY release is altered during the steroid-induced LH surge in ovariectomised (OVX) MA rats, and whether exogenous NPY initiates steroid-induced LH surge in OVX old rats. In the first study, NPY release from the ME-arcuate nucleus, as assessed by the push,pull cannula technique, was significantly increased before and during the progesterone-induced LH surge in oestrogen (E2)-primed ovariectomised young rats (2,3 months old). This antecedent increase in NPY release seen in young rats was not apparent in MA rats (11,13 months old) in association with a delayed and attenuated LH surge. In the second study, whereas progesterone failed to induce LH surges in E2 -primed ovariectomised old rats (23,25 months old), intracerebroventricular NPY (0.1,0.5 µg) injections at 1100, 1200 and 13.00 h resulted in LH surge induction in E2 + progesterone-primed ovariectomised old rats. Because increased hypothalamic NPY synthesis and release is obligatory for the preovulatory LH discharge in young rats, the present findings suggest that alteration in NPY release from the ME-arcuate nucleus contributes to the delayed and reduced LH surges in MA rats and may be involved in the subsequent loss of the LH surges in old rats. [source] Expression of AMPA Receptor Subunits (GluR1,GluR4) in Gonadotrophin-Releasing Hormone Neurones of Young and Middle-Aged Persistently Oestrous Rats During the Steroid-Induced Luteinising Hormone SurgeJOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2006J. D. Bailey Abstract Glutamate provides excitatory input to gonadotrophin-releasing hormone (GnRH) neurones and elicits a response indicative of AMPA receptors. To determine if and which AMPA subunits are expressed by GnRH neurones, we conducted triple-label immunohistochemistry and confocal analyses on tissue obtained at 08.00, 12.00, 16.00 and 20.00 h from young and middle-aged, persistently oestrous (MA-PE) rats that were ovariectomised and primed with oestrogen and progesterone to induce a luteinising hormone (LH) surge. Each AMPA subunit was found in GnRH neurones, but in different patterns across the diurnal cycle, which were influenced by age. GluR1 expression increased earlier in young rats and the percentage of Fos-positive GnRH neurones expressing GluR1 rose significantly and was sustained from 12.00,16.00 h. GluR1 expression was delayed in MA-PE rats and the percentage of Fos-positive GnRH neurones expressing GluR1 peaked at 20.00 h. GluR2 expression in GnRH neurones did not change over time and was not affected by age; however, the percentage of Fos-positive GnRH neurones expressing GluR2 increased earlier and was sustained from 08.00,16.00 h in young rats whereas, in MA-PE rats, this percentage peaked at 20.00 h. GluR3 expression also increased earlier in young rats and peaked at 12.00 h but was delayed in MA-PE rats and peaked at 20.00 h. The number of Fos-positive GnRH neurones that coexpressed GluR3 peaked at 12.00 h in young rats but showed little change from 12.00,20.00 h in MA-PE rats. GluR4 expression was maintained at higher levels at 08.00 and 12.00 h in young rats; although the percentage of Fos-positive GnRH neurones expressing GluR4 peaked at 12.00 h in young rats, it showed little change in MA-PE rats. In summary, our data show that a higher proportion of Fos-positive GnRH neurones coexpressed AMPA receptor subunits in young rats and the expression, particularly of GluR1 and GluR2, was increased and sustained throughout the surge, whereas GluR3 and GluR4 expression peaked just before. In MA-PE rats, the rate of expression of GluR subunits and Fos in GnRH neurones was altered in a manner that may explain the delay and attenuation of the LH surge. [source] Central GABAA but not GABAB Receptors Mediate Suppressive Effects of Caudal Hindbrain Glucoprivation on the Luteinizing Hormone Surge in Steroid-Primed, Ovariectomized Female RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 7 2005S. R. Singh Abstract The neurochemical mechanisms that link caudal hindbrain glucoprivic-,sensitive' neurones with the forebrain gonadotrophin-releasing hormone (GnRH)-pituitary luteinizing hormone (LH) axis remain unclear. Available studies indicate that the amino acid neurotransmitter, ,-aminobutyric acid (GABA), inhibits reproductive neuroendocrine function, and that caudal fourth ventricular administration of the glucose antimetabolite, 5-thioglucose (5TG), enhances GABA turnover within discrete septopreoptic structures that regulate LH secretion. The current experiments utilized the selective GABAA and GABAB receptor antagonists, bicuculline and phaclofen, as pharmacological tools to investigate whether one or both receptor subtypes function within neural pathways that suppress GnRH neuronal transcriptional activation and LH release during central glucose deficiency. During the ascending phase of the afternoon LH surge, groups of steroid-primed, ovariectomized female Sprague-Dawley rats were pretreated by lateral ventricular administration of bicuculline, phaclofen, or vehicle only, before fourth ventricular injection of 5TG or vehicle. The data indicate that, 2 h after 5TG treatment, Fos immunoexpression by rostral preoptic GnRH neurones and plasma LH levels were diminished relative to the vehicle-treated controls, and that inhibitory effects of 5TG on these parameters were attenuated by pretreatment with bicuculline, but not phaclofen. These results demonstrate that central GABAA, but not GABAB receptor stimulation during hindbrain glucoprivation, is required for maximal inhibition of reproductive neuroendocrine function by this metabolic challenge. The current studies thus reinforce the view that central GABAergic neurotransmission mediates regulatory effects of central glucoprivic signalling on the GnRH-pituitary LH axis. [source] Oestrogen Receptor , is Essential for Female-Directed Chemo-Investigatory Behaviour but is not Required for the Pheromone-Induced Luteinizing Hormone Surge in Male MiceJOURNAL OF NEUROENDOCRINOLOGY, Issue 2 2000S. R. Wersinger The expression of normal masculine sexual behaviour requires testosterone. Testosterone can bind to androgen receptors, either in its native form, or after reduction to other androgen metabolites. In addition, testosterone can be aromatized to oestrogen, and bind to oestrogen receptor , and/or ,. Male copulatory behaviour is deficient in mice lacking functional oestrogen receptor , gene (ER,KO mice). We sought to determine which aspect(s) of masculine sexual behaviour is compromised in the ER,KOs. Specifically, we asked whether ER,KO males have reduced motivation and/or an inability to recognize oestrous females. We found significant differences between mice of different genotypes in the amount of chemo-investigatory behaviour displayed and in the target of their investigation. Wild-type males spent more time investigating ovariectomized, oestradiol-treated females, than either males, or ovariectomized females that had not received hormone priming. ER,KO males spent little time investigating any of the stimulus mice and showed no preferences. To test the hypothesis that this lack of chemo-investigatory behaviour is due to the inability of ER,KO males to detect and respond to female pheromones, we exposed males to chemosensory cues (soiled bedding) from females. Males resided in clean, or female-soiled, cage bedding for 60 min. Next, blood was collected and plasma luteinizing hormone (LH) assayed. We also assessed Fos-like immunoreactivity (Fos-ir) in several neural regions involved in processing chemosensory cues. Despite the fact that male ER,KOs spend little time engaged in chemo-investigation of females, their neuroendocrine responses to female-soiled bedding were similar to those seen in wild-type males. Our data suggest that the normal coupling between the neuroendocrine response to females and the generation of sexual behaviour is disrupted in ER,KO mice. Responses to female pheromones do not require ER,. However, normal male sexual performance requires the ER, gene. [source] Daily rhythms and sex differences in vasoactive intestinal polypeptide, VIPR2 receptor and arginine vasopressin mRNA in the suprachiasmatic nucleus of a diurnal rodent, Arvicanthis niloticusEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2009M. M. Mahoney Abstract Diurnal and nocturnal animals differ with respect to the time of day at which the ovulatory surge in luteinizing hormone occurs. In some species this is regulated by the suprachiasmatic nucleus (SCN), the primary circadian clock, via cells that contain vasoactive intestinal polypeptide (VIP) and vasopressin (AVP). Here, we evaluated the hypothesis that chronotype differences in the timing of the luteinizing hormone surge are associated with rhythms in expression of the genes that encode these neuropeptides. Diurnal grass rats (Arvicanthis niloticus) were housed in a 12/12-h light,dark cycle and killed at one of six times of day (Zeitgeber time 1, 5, 9, 13, 17, 21; ZT 0 = lights-on). In-situ hybridization was used to compare levels of vip, avp and VIP receptor mRNA (vipr2) in the SCN of intact females, ovariectomized females, ovariectomized females given estradiol and intact males. We found a sex difference in vip rhythms with a peak occurring at ZT 13 in males and ZT 5 in intact females. In all groups avp mRNA rhythms peaked during the day, from ZT 5 to ZT 9, and had a trough in the dark at ZT 21. There was a modest rhythm and sex difference in the pattern of vipr2. Most importantly, the patterns of each of these SCN rhythms relative to the light,dark cycle resembled those seen in nocturnal rodents. Chronotype differences in timing of neuroendocrine events associated with ovulation are thus likely to be generated downstream of the SCN. [source] Elevated KiSS-1 Expression in the Arcuate Nucleus Prior to the Cyclic Preovulatory Gonadotrophin-Releasing Hormone/Lutenising Hormone Surge in the Ewe Suggests a Stimulatory Role for Kisspeptin in Oestrogen-Positive FeedbackJOURNAL OF NEUROENDOCRINOLOGY, Issue 10 2006K. M. Estrada Kisspeptins are encoded by the gene KiSS-1 and regulate gonadotrophin-releasing hormone (GnRH) and gonadotrophin secretion in various species, including humans. Here, we quantify gene expression of KiSS-1 in the arcuate nucleus (ARC) across the ovine oestrous cycle and demonstrate an increase in the caudal division of the ARC during the preovulatory period. These data strongly suggest that kisspeptins are involved in the generation of the preovulatory GnRH and luteinising hormone surge. [source] Three-Dimensional Representation of the Neurotransmitter Systems of the Human Hypothalamus: Inputs of the Gonadotrophin Hormone-Releasing Hormone Neuronal SystemJOURNAL OF NEUROENDOCRINOLOGY, Issue 2 2006B. Dudas Abstract The gonadotrophin-releasing hormone (GnRH) represents the final common pathway of a neuronal network that integrates multiple external and internal factors to control fertility. Among the many inputs GnRH neurones receive, oestrogens play the most important role. In females, oestrogen, in addition to the negative feedback, also exhibits a positive feedback influence upon the activity and output of GnRH neurones to generate the preovulatory luteinising hormone surge and ovulation. Until recently, the belief has been that the GnRH neurones do not contain oestrogen receptors and that the action of oestrogen upon GnRH neurones is indirect, involving several, oestrogen-sensitive neurotransmitter and neuromodulator systems that trans -synaptically regulate the activity of the GnRH neurones. Although this concept still holds for humans, recent studies indicate that oestrogen receptor-beta is expressed in GnRH neurones of the rat. This review provides three dimensional stereoscopic images of GnRH-immunoreactive (IR) and some peptidergic (neuropeptide Y-, substance P-, ,-endorphin-, leu-enkaphalin-, corticotrophin hormone-releasing- and galanin-IR) and catecholaminergic neurones and the communication of these potential oestrogen-sensitive neuronal systems with GnRH neurones in the human hypothalamus. Because the post-mortem human tissue does not allow the electron microscopic identification of synapses on GnRH neurones, the data presented here are based on light microscopic immunocytochemical experiments using high magnification with oil immersion, semithin sections or confocal microscopy. [source] Stimulation of Uterine Cell Cytokine Production By Ovarian HormonesAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 1 2000J.A. DELOIA PROBLEM: Although leukocytes do not possess significant numbers of ovarian steroid hormone receptors, their numbers in the endometrium vary consistently, relative to the menstrual cycle. The possibility that cell types within the endometrium express leukocyte-attracting genes in response to ovarian hormones was investigated. METHOD OF STUDY: Endometrial biopsies were collected 10 days post-leutinizing hormone surge; the cell types were separated and cultured individually for 5 days in the presence of increasing amounts of estrogen or progesterone. Following culture, RNA was collected from cells and reverse-transcription-polymerase chain reaction was used to determine relative levels of gene expression of monocyte chemotactic proteins (MCP)-1, -2, and -3, and interleukin (IL)-12p35 and p40. RESULTS: Although both endometrial stroma and glands were able to make MCP mRNA, steady-state levels of gene expression did not vary significantly relative to hormone treatment. The same was found for the p35 molecule of the IL-12 gene; however, differences were observed for the p40 subunit. CONCLUSIONS: Within the human endometrium, chemokines other than MCP and IL-12 are most likely responsible for cycle-related leukocyte recruitment. [source] Endocrinological and endometrial factors in recurrent miscarriageBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 12 2000T. C. Li Consultant Gynaecologist Objective To investigate the endocrinological and endometrial factors in women with unexplained recurrent miscarriage Design Prospective, case study Setting Recurrent miscarriage clinic, Jessop Hospital for Women, Sheffield Participants One hundred and forty-four women with unexplained recurrent (, 3) miscarriages Methods A blood sample was obtained in early follicular phase (day 3,5) to measure follicle stimulating hormone, luteinising hormone, prolactin, androgens and thyroid function; daily blood/urine samples were obtained from mid-follicular phase to measure luteinising hormone until the luteinising hormone surge was identified; endometrial biopsy and a further blood sample for progesterone measurement were obtained in the mid-luteal phase. A transvaginal ultrasonography was performed to evaluate ovarian morphology. Results Hypersecretion of luteinising hormone or ultrasonographic features of polycystic ovarian disease was present in 8% and 7.8% of women, respectively. The free androgen index was elevated in 14.6% of subjects. In the mid-luteal phase, low progesterone level was found in 17.4% and delayed endometrial development was noted in 27.1% of women. Although women with recurrent miscarriage women and delayed endometrium had significantly lower progesterone levels than those with normal endometrial development, only 8/24 had mid-luteal progesterone levels below 30 nmol/L. Recurrent miscarriage was not associated with hyperprolactinaemia or abnormal thyroid function test. Conclusions Endocrinological and endometrial abnormalities are present in about a quarter of women with unexplained recurrent miscarriage. [source] | ||||||||||