The Hypothalamic Control of the Menstrual Cycle and the Role of Endogenous Opioid Peptides

Ferin, Michel; Vugt, D. Van; Wardlaw, Sharon L.

doi:10.1016/b978-0-12-571140-1.50015-3

Cited by 186 publications

(126 citation statements)

References 114 publications

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“…The negative estrogen feedback might, thus, be exerted indirectly, via a subgroup of CRH neurons. CRH has been reported to suppress GnRH secretion through a direct and an indirect, arcuate nucleus proopiomelanocortin/13-endorphin-mediated path ( 15,54).…”

Section: Resultsmentioning

confidence: 99%

Evidence of direct estrogenic regulation of human corticotropin-releasing hormone gene expression. Potential implications for the sexual dimophism of the stress response and immune/inflammatory reaction.

Vamvakopoulos

Chrousos²

1993

J. Clin. Invest.

407

206

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Corticotropin-releasing hormone (CRH) plays major roles in coordination of the stress response and regulation of the immune/inflammatory reaction, two important functions associated with sexual dimorphism. Two overlapping segments of the 5' flanking region of the human (h) CRH gene, the proximal 0.9 kb (containing two perfect half-palindromic estrogenresponsive elements IEREsI) and the 2.4 kb (including the former and containing two additional perfect half-palindromic EREs), were examined for their ability to confer estrogen-mediated transcriptional enhancement to a homologous or heterologous promoter. The level of estrogen-induced transactivation by the 0.9-and 2.4-kb segments was determined by chloramphenicol acetyltransferase analysis in CV-1 cells cotransfected with estrogen receptor (ER) cDNA expression plasmids, and found to be respectively -10% and 20% of that of the strongly estrogen-responsive Xenopus vitellogenin A2 enhancer. Gel retardation and immunoprecipitation demonstrated specific association between the perfect half-palindromic EREs of hCRH gene and the DNA binding domain of hER in vitro. These findings may constitute the basis of sexual dimorphism in the expression of the CRH gene in the central nervous system and periphery, and might shed light in existing gender differences in stress response and immune regulation. (J. Clin. Invest.

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Section: Resultsmentioning

confidence: 99%

Evidence of direct estrogenic regulation of human corticotropin-releasing hormone gene expression. Potential implications for the sexual dimophism of the stress response and immune/inflammatory reaction.

Vamvakopoulos

Chrousos²

1993

J. Clin. Invest.

407

206

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“…The general approach is analogous to the use of naloxone, an opiate receptor blocker, to determine endogenous endorphin "tone" (13,14). The use of this tool for discriminating between different physiologic states requires a precision in measurement that is demonstrated in these studies.…”

Section: Discussionmentioning

confidence: 99%

“…This principle derives from quantitative theories of drug action (12) and has proven extremely useful in determination of opioid tone using the opiate receptor blocker, naloxone (13,14). We have applied an analogous approach to the assessment of the overall amount of GnRH secreted by using a GnRH antagonist that competitively blocks the GnRH receptor and LH secretion as the marker of GnRH action.…”

Section: Introductionmentioning

confidence: 99%

Decreased release of gonadotropin-releasing hormone during the preovulatory midcycle luteinizing hormone surge in normal women.

Hall

Taylor²,

Rivier³

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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To investigate the contribution of hypothalamic gonadotropin-releasing hormone (GnRH) secretion to the midcyde gonadotropin surge in the human, the response of luteniZing hormone (LH) to competitive GnRH receptor blockade achieved by administration of a range of doses of a pure GnRH antagonist was used to provide a semiquantitative estimate of endogenous GnRH secretion. The LH response to 5, 15, 50, and 150 iag/kg s.c. of the NAL-GLU GnRH antagonist ',D-4CIPhe2,D-Pal3,Arg5,D-4-p-methoxybenzoyl-2-aminobutyric acid'6,D-Ala1O'GnRH, where 2Nal is 2-naphthylalanine, 4CIPhe is 4-chlorophenylalanine, and 3Pal is 3-pyridylabnine) was measured in normal women in the early and late follicular phases of the menstrual cycle, at the time of the midcycle LH surge and in the early luteal phase. LH decreased in a dose-response fashion after administration of the GnRH antagonist in aUi cycle phases (P < 0.0001 Direct measurements of GnRH in pituitary portal blood indicate that a surge of GnRH secretion is generally associated with spontaneous and sex steroid-induced gonadotropin surges in sheep (4-6). GnRH levels also appear to increase at the time of the proestrus surge in rats (7) and rhesus monkeys (8, 9). These direct techniques of accessing information regarding the hypothalamic component of the preovulatory surge are clearly not feasible in the human and measurements of GnRH in the peripheral circulation do not accurately reflect hypothalamic GnRH secretion ifat all (10). Therefore, an understanding of the physiology of GnRH secretion and pituitary responsiveness to this releasing hormone in the human can only be achieved by combining a number of indirect approaches. Monitoring of pulsatile LH secretion can provide insight into the frequency of GnRH secretory episodes (11) but does not permit estimates to be made ofthe amount of GnRH secreted. The dose of exogenous pulsatile GnRH required to mimic normal menstrual cycles and a normal midcycle surge in GnRH-deficient women (3) has been determined empirically, by comparison with "target"or reference ranges derived from studies in normal women, but does not provide information about potential changes in the actual quantity of endogenous GnRH secreted under various physiologic conditions in the intact human.A competitive receptor antagonist can be used to assess the relative amount of an unmeasurable endogenous ligand by determining the susceptibility of a marker of its action to specific blockade. This principle derives from quantitative theories of drug action (12) and has proven extremely useful in determination of opioid tone using the opiate receptor blocker, naloxone (13,14). We have applied an analogous approach to the assessment of the overall amount of GnRH secreted by using a GnRH antagonist that competitively blocks the GnRH receptor and LH secretion as the marker of GnRH action. The underlying assumption is that the amount ofGnRH present at a given time is directly proportional to the dose of GnRH antagonist required to inhibit LH secretion. 2Nal is 2-napht...

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“…The reduction of this inhibition is necessary for the preovulatory surge of LH (Spijkstra et al, 1988;Walsh and Clarke, 1998). Gonadal steroids also exert an inhibitory effect on gonadotropin secretion (negative feedback action) and this effect is mediated (at least in part) by an increase in the opioidergic tone of the hypothalamus which is the cause of decreased GnRH secretion and a subsequent reduction of LH release (Ferin et al, 1984;Melis et al, 1984). Sex steroids influence the number of the brain opioid receptors (Casulari et al, 1987;Martini et al, 1989) and their binding characteristic (Piva et al, 1995;Thom et al, 1996).…”

mentioning

confidence: 99%

Steroid effects on the in vitro LH secretion from pituitary cells of sexually immature carp (Cyprinus carpio L.) under the influence of naltrexone and morphine

Sokolowska-Mikolajczyk¹,

Socha²,

Epler³

2010

CZECH J ANIM SCI

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Dispersed cells from sexually immature carp (footlings) pituitaries were exposed to estradiol (E2) or testosterone (T) (both at 3 × 10–8 M) in the presence of opioid receptor antagonist naltrexone (10–8 or 10–6 M) and/or agonist – morphine (10–8 or 10–6 M). Naltrexone alone at 10–6 M increased the LH level as compared with the control. Morphine (10–8 or 10–6 M), T and E2 had no influence on LH levels. The combination of T with naltrexone (10–8 M) stimulated LH release if compared with the control or with T alone. Morphine (both concentrations) with T caused significantly higher LH secretion than the control medium and T alone. Estradiol with naltrexone (10–8 and 10–6 M) had no influence on LH concentration. In media with E2 and morphine (10–8 M) LH levels were higher than in the control and estradiol alone. The results show that in common carp sex steroids affect the response of pituitary cells to opioid agonist or antagonist giving an evidence on the role of steroids in LH release mediated by the opioid system.

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The Hypothalamic Control of the Menstrual Cycle and the Role of Endogenous Opioid Peptides

Cited by 186 publications

References 114 publications

Evidence of direct estrogenic regulation of human corticotropin-releasing hormone gene expression. Potential implications for the sexual dimophism of the stress response and immune/inflammatory reaction.

Evidence of direct estrogenic regulation of human corticotropin-releasing hormone gene expression. Potential implications for the sexual dimophism of the stress response and immune/inflammatory reaction.

Decreased release of gonadotropin-releasing hormone during the preovulatory midcycle luteinizing hormone surge in normal women.

Steroid effects on the in vitro LH secretion from pituitary cells of sexually immature carp (Cyprinus carpio L.) under the influence of naltrexone and morphine

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