scholarly journals Intra-pituitary regulation of gonadotrophs in male rodents and primates

Reproduction ◽  
2004 ◽  
Vol 128 (1) ◽  
pp. 13-23 ◽  
Author(s):  
Stephen J Winters ◽  
Joseph P Moore
Keyword(s):  
Species Differences ◽  
Receptor Gene ◽  
Gnrh Receptor ◽  
Male Rats ◽  
Pituitary Cells ◽  
Α Subunit ◽  
Folliculostellate Cells ◽  
Autocrine Regulation ◽  
Subunit Expression ◽  
Receptor Gene Expression

Paracrine and autocrine regulation is well established in many organs including the gonads, but the notion of communication among pituitary cells is a relatively new concept. The FSH-β and GnRH-receptor genes are up-regulated by pituitary activin and down-regulated by pituitary follistatin, and circulating inhibin disrupts this local regulation by functioning as an endogenous competitor of the activin receptor. Activin and follistatin production by folliculostellate cells may play a central role in these responses. α-Subunit expression is maintained at high levels in the absence of GnRH through unknown mechanisms. There is evidence that the intra-pituitary regulation of FSH-β and GnRH-receptor gene expression may activate pubertal maturation in male rats. Finally, there are marked differences in follistatin expression and its regulation by GnRH and androgens in male primates and rats that appear to explain species differences in the differential secretion of FSH and LH, although the physiological significance of these differences is not yet known.

Mammary gland-specific regulation of GNRH and GNRH-receptor gene expression is likely part of a local autoregulatory system in female vizcachas (Rodentia: Chinchillidae)

2020 ◽  
Vol 296 ◽  
pp. 113518
Author(s):  
María Clara Corso ◽  
Santiago Andrés Cortasa ◽  
Alejandro Raúl Schmidt ◽  
Sofía Proietto ◽  
Pablo Ignacio Felipe Inserra ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Receptor Gene ◽  
Gnrh Receptor ◽  
Specific Regulation ◽  
Receptor Gene Expression

scholarly journals The Gonadotropins Subunits, GNRH and GNRH Receptor Gene Expression and Role of Carbon Monoxide in Seasonal Breeding Animals

2012 ◽  
Vol 12 (1) ◽  
pp. 15-23
Author(s):  
Maria Romerowicz-Misielak ◽  
Marek Koziorowski
Keyword(s):  
Gene Expression ◽  
Carbon Monoxide ◽  
Receptor Gene ◽  
Hormone Secretion ◽  
Gnrh Receptor ◽  
Day Length ◽  
Seasonal Breeding ◽  
Receptor Gene Expression ◽  
Main Factor

The Gonadotropins Subunits, GNRH and GNRH Receptor Gene Expression and Role of Carbon Monoxide in Seasonal Breeding AnimalsSeasonality in reproduction occurs mainly in wild species and it is the result of natural selection. Signals to start or finish the period of reproductive activity, both environmental and hormonal depend on the neuroendocrine pathway - synthesis and secretion of pituitary hormones, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), under the control of the hypothalamic gonadotropin-releasing hormone (GnRH) neurons. Variable frequency of GnRH pulses is not only the main factor governing primary and preovulatory release of gonadotropins, but it can also play a role in the specific transcriptional activity of gonadotropin subunit genes (LHβ, FSHβ and Cga). However, changes in release of GnRH pulse pattern do not explain the preferential stimulation of the synthesis and secretion of gonadotropins in the annual reproductive cycle. In this regulation also a GnRH independent mechanism participates. It seems that the main factor responsible for the occurrence of the seasonal modulation of reproduction in sheep and other mammals, is significant changes in response of GnRH systems to gonadal steroids. The effect of carbon monoxide on regulation of the hypothalamic-pituitary-gonadal axis has not been studied to date. There is substantial evidence to suggest that it may play a role in the transduction of information on day length. The presence of heme oxygenase-2 in hypothalamic areas important for regulation of pituitary secretory function and in the pituitary itself suggests that carbon monoxide, the product of this enzyme, may participate in the regulation of hormone secretion by the pineal gland.

scholarly journals Effects of dehydration on endocrine regulation of the electrolyte and fluid balance and atrial natriuretic peptide-binding sites in perinatally malnourished adult male rats

2002 ◽  
pp. 835-848 ◽  
Author(s):  
N Sebaai ◽  
J Lesage ◽  
A Alaoui ◽  
JP Dupouy ◽  
S Deloof
Keyword(s):  
Gene Expression ◽  
Binding Sites ◽  
Water Deprivation ◽  
Receptor Gene ◽  
Plasma Osmolality ◽  
Significant Rise ◽  
Male Rats ◽  
Receptor Density ◽  
D Values ◽  
Receptor Gene Expression

OBJECTIVE: The first aim of this work was to investigate, under basal conditions in adult male rats, the long-term consequences of perinatal maternal food restriction on the plasma concentrations of vasopressin (VP), aldosterone and atrial natriuretic peptide (ANP) and on plasma renin activity (PRA). Furthermore, under these same conditions, the hypothalamic VP gene expression as well as the density (B(max)), affinity (K(d)) and gene expression of ANP receptors were determined in kidneys and adrenals. The second aim of this work was to examine the responsiveness to dehydration in perinatally malnourished rats. Thus, the latter parameters were studied in these rats after 72 h water deprivation. METHODS: This study was conducted on 4-Month-old male rats from mothers exposed to 50% food restriction (FR50) during the last week of gestation and lactation and on age-matched control animals (C). At this stage, both C and FR50 rats were killed by decapitation between 0900 h and 1000 h in order to determine parameters under basal conditions or after 72 h water deprivation. Plasma VP, ANP and aldosterone levels and PRA were determined by radioimmunoassay. Hypothalamic VP gene expression was determined in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) by in situ hybridization. The B(max) and K(d) values of ANP receptors were evaluated from Scatchard plots. ANP receptor gene expression was determined by Northern blot analysis. RESULTS: Under basal conditions, perinatal malnutrition reduced body weight, absolute weight of kidneys and adrenals, and haematocrit. Compared with control rats, FR50 rats had significantly greater plasma VP and aldosterone levels but PRA, plasma ANP levels, plasma osmolality and hypothalamic VP gene expression were not significantly different. Perinatal malnutrition did not significantly affect glomerular ANP receptor density, but in adrenals it decreased both B(max) and K(d) values of ANP-B receptors (biological receptors) and increased B(max) of ANP-C receptors (clearance receptors). ANP-B(A) (receptor subtype A of ANP-B receptors) receptor gene expression was not significantly affected, whereas ANP-C receptor gene expression was enhanced in both adrenals and kidneys in FR50 rats. After 72 h dehydration, control rats showed a significant rise in haematocrit, plasma osmolality, PRA, circulating levels of VP and aldosterone and VP gene expression in both PVN and SON but showed a decrease in plasma ANP levels. B(max) of ANP-B receptors was decreased whereas B(max) of ANP-C receptors was enhanced in both adrenals and kidneys. ANP-B(A) receptor gene expression was not significantly affected in either kidneys or adrenals in dehydrated control rats. Similarly, ANP-C receptor gene expression was unaffected in kidneys whereas it was significantly enhanced in adrenals. In FR50 rats, the effects of water deprivation were qualitatively similar to those reported in controls concerning plasma parameters except for plasma VP levels which tended to rise (not significant) but this increase was only very slight compared with controls. Moreover, unlike controls, VP gene expression in both PVN and SON was not enhanced after dehydration in FR50 rats. In kidneys, dehydrated FR50 rats, like controls, upregulated ANP-C receptors, but they were unable to downregulate ANP-B receptors. In adrenals, unlike controls, FR50 rats enhanced ANP-B receptor density whereas they decreased both ANP-C receptor density and expression after 72 h dehydration. Similar to controls, the expression of ANP-B(A) receptors in both kidneys and adrenals as well as the expression of ANP-C receptors in kidneys, were unaffected in dehydrated FR50 rats. CONCLUSION: Perinatal malnutrition had long-lasting effects on regulation of the fluid and electrolyte balance under basal conditions. The main effects were a significant rise in circulating levels of VP and aldosterone, and changes in density of adrenal ANP-binding sites and ANP-C receptor gene expression in both adrenals and kidneys. Perinatal malnutrition also affects the responsiveness to water deprivation with alterations in both hypothalamic VP gene expression and regulation of ANP-binding sites.

scholarly journals Resistance of Hypogonadic Patients with Mutated GnRH Receptor Genes to Pulsatile GnRH Administration

1999 ◽  
Vol 84 (3) ◽  
pp. 990-996 ◽  
Author(s):  
Philippe Caron ◽  
Stéphanie Chauvin ◽  
Sophie Christin-Maitre ◽  
Antoine Bennet ◽  
Najiba Lahlou ◽  
...  
Keyword(s):  
Transmembrane Domain ◽  
Receptor Gene ◽  
Hypogonadotropic Hypogonadism ◽  
Chinese Hamster ◽  
Gnrh Receptor ◽  
Primary Amenorrhea ◽  
Recessive Trait ◽  
Intracellular Loop ◽  
Α Subunit ◽  
Pulsatile Gnrh

We have studied a kindred with three siblings with isolated hypogonadotropic hypogonadism caused by compound heterozygote mutations in the GnRH receptor gene. The disorder was transmitted as an autosomal recessive trait. The R262Q mutation in intracellular loop 3 of the receptor was associated with a mutation in the third transmembrane domain of the receptor, A129D, that has never been described before. This A129D mutation results in a complete loss of function, indicated by the lack of inositol triphosphate (TP3) 3 production by transfected Chinese hamster ovary (CHO) cells after GnRH stimulation. The two brothers had microphallus and bilateral cryptorchidism and were referred for lack of puberty, whereas their sister had primary amenorrhea and a complete lack of puberty. Their basal gonadotropin concentrations were below the reference range, and their endogenous LH secretory patterns were abnormal, with a low-normal frequency of small pulses or no apparent LH pulse. Pulsatile GnRH administration (10 μg/pulse every 90 min for 40 h) resulted in increased mean LH without any significant changes in testosterone levels in the two brothers, whereas the LH secretory profile of their sister remained apulsatile. Larger pulses of exogenous GnRH (20 μg every 90 min for 24 h) caused the sister to produce recognizable low amplitude LH pulses. The concentrations of free α-subunit significantly increased in all patients during the pulsatile GnRH administration. Thus, these hypogonadal patients are partially resistant to pulsatile GnRH administration, suggesting that they should be treated with gonadotropins to induce spermatogenesis or ovulation rather than with pulsatile GnRH.

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