Gonadotrophin Release in Hypogonadal and Normal Mice After Electrical Stimulation of the Median Eminence or Injection of Luteinizing Hormone Releasing Hormone

Iddon, Carol A.; Charlton, H. M.; Fink, George

doi:10.1677/joe.0.0850105

Cited by 27 publications

(12 citation statements)

References 6 publications

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“…Implantation of an oestradiol-containing capsule had no significant effect on pituitary LH content or concentration in either hpg or normal mice. In order to economize on animals, control groups in which animals were injected with LH-RH followed by saline and vice versa were not included because previous studies in mice showed that sequential blood sampling either in untreated or saline-injected animals did not significantly alter plasma LH concentrations (Iddon, Charlton & Fink, 1980) and in rats the priming effect of LH-RH could not be elicited by injecting LH-RH followed by saline or vice versa (Aiyer et al 1974;Fink & Pickering, 1980). The reason for the difference in dosage of LH-RH required to produce a clear-cut and reproducible LH release in the present study compared with that used by Iddon et al (1980) is not readily apparent, although Iddon et al (1980) used male mice.…”

Section: Resultsmentioning

confidence: 99%

Priming effect of luteinizing hormone releasing hormone in the hypogonadal mouse

Fink¹,

Sheward²,

Charlton³

1982

Journal of Endocrinology

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We have investigated the LH response to LH releasing hormone (LH-RH) in female hypogonadal (hpg) mice in which the hypothalamus contains no LH-RH and the pituitary gland contains significantly less LH than in normal mice. Both the releasing action and the priming effect of LH-RH were not significantly different in hpg compared with normal mice. Raised plasma concentrations of oestradiol-17 beta reduced pituitary responsiveness to LH-RH in normal but not in hpg mice. These results show that in the mouse neither long-term exposure to normal levels of LH-RH nor a normal pituitary content of LH are necessary for either the releasing or the priming action of LH-RH.

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Section: Resultsmentioning

confidence: 99%

Priming effect of luteinizing hormone releasing hormone in the hypogonadal mouse

Fink¹,

Sheward²,

Charlton³

1982

Journal of Endocrinology

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“…For example, in the hypogonadal (hpg) mouse it was observed that administration of 40 ng of a GnRH analog could immediately trigger LH secretion from the pituitary, albeit significantly lower than that in normal mice [62]. In the rhesus monkey (Macaca mulatta), the responsiveness of pituitary gonadotropes to GnRH stimulation is clearly enhanced by a preceding chronic pulsatile infusion of GnRH [63].…”

Section: Kiss1r Displays Basal Constitutive Signaling and Kp-independmentioning

confidence: 99%

KISS1R: Hallmarks of an Effective Regulator of the Neuroendocrine Axis

Millar

Babwah

2015

Neuroendocrinology

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Kisspeptin (KP) is now well recognized as a potent stimulator of gonadotropin-releasing hormone (GnRH) secretion and thereby a major regulator of the neuroendocrine-reproductive axis. KP signals via KISS1R, a G protein-coupled receptor (GPCR) that activates the G proteins Gα_q/11. Modulation of the interaction of KP with KISS1R is therefore a potential new therapeutic target for stimulating (in infertility) or inhibiting (in hormone-dependent diseases) the reproductive hormone cascade. Major efforts are underway to target KISS1R in the treatment of sex steroid hormone-dependent disorders and to stimulate endogenous hormonal responses along the neuroendocrine axis as part of in vitro fertilization protocols. The development of analogs modulating KISS1R signaling will be aided by an understanding of the intracellular pathways and dynamics of KISS1R signaling under normal and pathological conditions. This review focuses on KISS1R recruitment of intracellular signaling (Gα_q/11- and β-arrestin-dependent) pathways that mediate GnRH secretion and the respective roles of rapid desensitization, internalization, and recycling of resensitized receptors in maintaining an active population of KISS1R at the cell surface to facilitate prolonged KP signaling. Additionally, this review summarizes and discusses the major findings of an array of studies examining the desensitization of KP signaling in man, domestic and laboratory animals. This discussion highlights the major effects of ligand efficacy and concentration and the physiological, developmental, and metabolic status of the organism on KP signaling. Finally, the potential for the utilization of KP and analogs in stimulating and inhibiting the reproductive hormone cascade as an alternative to targeting the downstream GnRH receptor is discussed.

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“…That the mutation results in an absence of endogenous GnRH secretion has been demonstrated by experiments in which injection of synthetic GnRH increases pituitary content and circulating levels of gonadotropin, as well as gonadal weight (Fink et al, 1982;Young et al, 1983), while electrical stimulation of the hypothalamus has no effect (Iddon et al, 1980). This mutant has been used by several investigators as a model to study the anatomy and physiology of the hypothalamic GnRH system.…”

Section: The Hypogonadal Mousementioning

confidence: 99%

Hormonal and neurotransmitter regulation of GnRH gene expression and related reproductive behaviors

et al. 1996

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Gonadotropin-releasing hormone (GnRH), having a highly conserved structure across mammalian species, plays a pivotal role in the control of the neuroendocrine events and the inherent sexual behaviors essential for reproductive function. Recent advances in molecular genetic technology have contributed greatly to the investigation of several aspects of GnRH physiology, particularly steroid hormone and neurotransmitter regulation of GnRH gene expression. Behavioral studies have focused on the actions of GnRH in steroid-sensitive brain regions to understand better its role in the facilitation of mating behavior. To date, however, there are no published reports which directly correlate GnRH gene expression and reproductive behavior. The intent of this article is to review the current understanding of the way in which changes in GnRH gene expression, and modifications of GnRH neuronal activity, may ultimately influence reproductive behavior.

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Gonadotrophin Release in Hypogonadal and Normal Mice After Electrical Stimulation of the Median Eminence or Injection of Luteinizing Hormone Releasing Hormone

Cited by 27 publications

References 6 publications

Priming effect of luteinizing hormone releasing hormone in the hypogonadal mouse

Priming effect of luteinizing hormone releasing hormone in the hypogonadal mouse

KISS1R: Hallmarks of an Effective Regulator of the Neuroendocrine Axis

Hormonal and neurotransmitter regulation of GnRH gene expression and related reproductive behaviors

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