Hypothalamic control of gonadotropin secretion

McCann, Samuel M.; Karanth, Sharada; Mastronardi, Claudio A.; Dees, W. Les; Childs, Gwen V.; Miller, Brian T.; Sower, Stacia A.; Yu, Wen H.

doi:10.1016/s0079-6123(02)41090-4

Cited by 21 publications

(19 citation statements)

References 59 publications

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“…The restoration of hypothalamic LHRH by both vitamin E doses paired with ethanol feeding indicates that vitamin E overcame the ethanol-induced secretory blockade. The lack of concordance between LH and FSH has been seen before and McCann and colleagues have long suggested the possibility that there is a hypothalamic FSH releasing factor separate from LHRH [15]. The additional possibility that the inhibin/activin system is involved is also worth consideration.…”

Section: Hypothalamusmentioning

confidence: 98%

Vitamin E prevents ethanol-induced inflammatory, hormonal, and cytotoxic changes in reproductive tissues

Zhu

Emanuele

LaPaglia

et al. 2007

Endocr

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Ethanol causes decreased function of the hypothalamic-pituitary-gonadal (HPG) axis. Ethanol resulted in inflammatory changes in HPG manifested by increased concentrations of pro-inflammatory cytokines. Since, such cytokines have deleterious effects on functions of HPG, it seemed possible that ethanol's suppressive action could be due, at least in part, to this inflammation. Since oxidative stress can cause inflammation, we have used the antioxidant vitamin E to test, whether reducing inflammation might protect reproductive functions from ethanol. Rats were fed an ethanol diet or pair fed identically without ethanol for a 3-week period. For the last 10 days, animals were given 30 IU/kg or 90 IU/kg or vehicle. Ethanol significantly increased hypothalamic, pituitary and testicular TNF-alpha and IL-6, all changes prevented by the higher dose of vitamin E. Also, ethanol induced changes in LHRH, LH, testosterone, and testicular germ cell apoptosis were similarly prevented by vitamin E. These data strikingly show that vitamin E protects the HPG from deleterious effects of ethanol and suggests that the mechanism of this protection might be both anti-inflammatory and antioxidant.

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Section: Hypothalamusmentioning

confidence: 98%

Vitamin E prevents ethanol-induced inflammatory, hormonal, and cytotoxic changes in reproductive tissues

Zhu

Emanuele

LaPaglia

et al. 2007

Endocr

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“…In contrast to its effect on LH secretion, the FSH response to kisspeptin is comparatively delayed and less robust in humans and rats. (59,63,65) This may be due to differences in secretory patterns of the gonadotrophins, (66) different gonadotroph responses to kisspeptins (65,67) or different feedback signals to the gonadotrophs (e.g. inhibin).…”

Section: Regulation Of Gnrhmentioning

confidence: 99%

Kisspeptin signalling and its roles in humans

Tng

2015

smedj

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Kisspeptins are a group of peptide fragments encoded by the KISS1 gene in humans. They bind to kisspeptin receptors with equal efficacy. Kisspeptins and their receptors are expressed by neurons in the arcuate and anteroventral periventricular nuclei of the hypothalamus. Oestrogen mediates negative feedback of gonadotrophin-releasing hormone secretion via the arcuate nucleus. Conversely, it exerts positive feedback via the anteroventral periventricular nucleus. The sexual dimorphism of these nuclei accounts for the differential behaviour of the hypothalamic-pituitary-gonadal axis between genders. Kisspeptins are essential for reproductive function. Puberty is regulated by the maturation of kisspeptin neurons and by interactions between kisspeptins and leptin. Hence, kisspeptins have potential diagnostic and therapeutic applications. Kisspeptin agonists may be used to localise lesions in cases of hypothalamic-pituitary-gonadal axis dysfunction and evaluate the gonadotrophic potential of subfertile individuals. Kisspeptin antagonists may be useful as contraceptives in women, through the prevention of premature luteinisation during in vitro fertilisation, and in the treatment of sex steroid-dependent diseases and metastatic cancers.

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“…Whether EGFP Ϫ neurons represent a second population of septal-preoptic hypothalamic GnRH neurons, which synthesize a distinct GnRH gene product as in advance teleost and in the guinea pig (15,34), or contain a posttranscriptionally modified hydroxyprolinated GnRH molecule (35) or GnRH fragments rather than fully mature GnRH1 (8) whose spatiotemporal origin might be different from the placodal origin of GnRH1 neurons (8)(9)(10)15) remains to be determined because a genomewide search failed to detect homologies to GnRH2, GnRH3, and lamprey III GnRH peptide or their ORFs in the rat and mouse databases (36). Therefore, GnRH2, GnRH3, and lamprey III GnRH immunoreactivity in the brain of rodents (16,17,37) is questionable, and the role of lamprey III GnRH in the control of follicle-stimulating hormone is debatable (37,38).…”

Section: Septal-preoptic Hypothalamus Egfp ؉ ͞Gnrhmentioning

confidence: 99%

Nonmammalian gonadotropin-releasing hormone molecules in the brain of promoter transgenic rats

Parhar

Soga²,

Ogawa³

et al. 2005

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

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Mammalian gonadotropin-releasing hormone (GnRH1) and nonmammalian immunoreactive GnRH subtypes were examined in transgenic rats carrying an enhanced GFP (EGFP) reporter gene driven by a rat GnRH1 promoter. Double-label immunocytochemistry was performed on EGFP ؉ ͞GnRH1 brain sections by using antisera against GnRH1, GnRH2 (chicken II), GnRH3 (salmon), or seabream GnRH. EGFP ؉ ͞GnRH1 neurons were in the septalpreoptic hypothalamus but not in the midbrain, consistent with GnRH1-immunopositive neurons in WT rats. Apparent coexpression of EGFP ؉ ͞GnRH1 with other GnRH subtypes was observed. All EGFP ؉ neurons in the septal-preoptic hypothalamus were GnRH1-immunopositive. However, only Ϸ80% of GnRH1-immunopositive neurons were EGFP ؉ , which awaits further elucidation. GnRH subtypes-immunopositive fibers and EGFP ؉ ͞GnRH1 fibers were conspicuous in the organum vasculosum of the lamina terminalis, median eminence, and surrounding the ependymal walls of the third ventricle and the aqueduct in the midbrain. These results demonstrate that the expression of the EGFP-GnRH1 transgene is restricted to the bona fide GnRH1 population and provide clear morphological evidence supporting the existence of GnRH1 neuronal subpopulations in the septal-preoptic hypothalamus, which might be driven by different segments of the GnRH promoter. This genetic construct permits analyses of promoter usage in GnRH neurons, and our histochemical approaches open questions about functional relations among isoforms of this peptide, which regulates reproductive physiology in its behavioral and endocrine aspects.luteinizing hormone-releasing hormone ͉ double-label immunocytochemistry ͉ green fluorescent protein ͉ hypothalamus ͉ preoptic area

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Hypothalamic control of gonadotropin secretion

Cited by 21 publications

References 59 publications

Vitamin E prevents ethanol-induced inflammatory, hormonal, and cytotoxic changes in reproductive tissues

Vitamin E prevents ethanol-induced inflammatory, hormonal, and cytotoxic changes in reproductive tissues

Kisspeptin signalling and its roles in humans

Nonmammalian gonadotropin-releasing hormone molecules in the brain of promoter transgenic rats

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