Presence and activity of LH-RH in the mid-term human fetus

Gilmore, D. P.; Dobbie, H. Gordon; McNeilly, A. S.; Mortimer, C. H.

doi:10.1530/jrf.0.0520355

Cited by 14 publications

(2 citation statements)

References 6 publications

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“…Our term placental qPCR data confirmed the presence of high levels of GnRH1, but no GnRH2. Previous studies have also shown high level of GnRH1 in the fetal circulation and the placenta is the likely source for this hormone (Aksel and Tyrey,1977; Gilmore et al,1978; Siler-Khodr and Khodr,1978). On the other hand, the fetal adrenal itself expressed high levels of GnRH2, whose cellular site of expression requires to be determined by further analysis.…”

Section: Discussionmentioning

confidence: 91%

G protein-coupled receptor expression in the adult and fetal adrenal glands

Xing

Nakamura

Rainey

2009

Molecular and Cellular Endocrinology

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Hormonal regulation of adrenal function occurs primarily through G protein-coupled receptors (GPCR), which may play different roles in fetal vs. adult adrenal glands. In this study, we compared the transcript levels of GPCR between fetal and adult adrenal and found that gonadotropin-releasing hormone receptor (GnRHR), latrophilin 3 receptor, G protein-coupled receptor 37, angiotensin II receptor type 2, latrophilin 2 receptor and melanocortin receptor were expressed at significant higher levels in fetal adrenal. High GnRHR protein expression was also detected in fetal adrenal using immunohistochemical analysis. To define potential ligand sources for fetal adrenal GnRHR, we demonstrated that GnRH1 mRNA was expressed at high levels in the placenta, while fetal adrenal had high expression of GnRH2. In summary, certain GPCR particularly GnRHR were highly expressed in fetal adrenal and the expression of GnRH mRNA in the placenta and the fetal adrenal raises the possibility of endocrine and/or paracrine/autocrine influence on fetal adrenal function. However, the exact function of GnRHR in fetal adrenal remains to be determined.

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Section: Discussionmentioning

confidence: 91%

G protein-coupled receptor expression in the adult and fetal adrenal glands

Xing

Nakamura

Rainey

2009

Molecular and Cellular Endocrinology

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“…Soon after, the primitive fiber tracts 25, 164 and the different hypothalamic nuclei (premammillary, preoptic, supraoptic, paraventricular, dorsomedial, arcuate and mammillary) are progressively differentiating between 6 and 12 weeks 88. As soon as the hypothalamic sulcus is recognizable (5th week) and well before the full differentiation of the hypothalamus (14 weeks), hypothalamic hormones, GnRH, thyrotropin releasing hormone (TRH) becomes detectable (5 6 and 8 weeks respectively), as well as somatostatin (SRIF) 4,8,32,33,86,169,205,207,241 Hypothalamic content and concentration of GnRH rise 10 to 15-fold from 6-8 week to midgestation, and despite conflicting reports 4, 42, 135, 205 do not show significant sex differences and appear to decline during the last trimester 13s, 2o5. Neurotransmitters, dopamine 151, serotonin and norepinephrine 24, 107, 161 have been found in fetal hypothalamus 9-12 weeks old, but their earlier presence is not excluded.…”

Section: The Hypothalamusmentioning

confidence: 99%

Sexual maturation of the hypothalamus: Pathophysiological aspects and clinical implications

Forest

1985

Acta neurochir

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Sexual maturation in humans begins early in fetal life and culminates in adulthood when the gonads have acquired a full capacity for reproduction. It is remarkable that during this long process, the pituitary gonadal function, hence its hypothalamic control presents an alternative of activation and inhibition periods, during which the interrelations of the 3 components of the hypothalamic-pituitary-gonadal axis change gradually and inversely. The ontogeny of the hypothalamic-pituitary system, the varying activity of the reproductive endocrine system throughout sexual maturation and the developmental changes in the interrelations of the hypothalamic-pituitary-gonadal axis are reviewed: the most striking feature of human sexual development is the long inhibition of hypothalamo-pituitary function during childhood. Much indirect evidence points to the determining role of the CNS in the maturation of hypothalamic function: the occurrence of rhythms of secretion, the amplitude of secretions and peripubertal specific sleep-related nycthemeral rhythm of secretion at the onset of puberty. Despite the reality of a negative feedback control, these changes do occur independently of gonadal secretions since they are observed (qualitatively if not strictly quantitatively) in agonadal children. It is likely that neurotransmitters (dopamine, serotonine) and opiates have an inhibitory effect on Gn-RH release. But we still don't know their evolution during sexual maturation. It does not appear that melatonine plays any determinant role in the onset of human puberty. The clinical implications of our present understanding of the physiological events occurring during sexual maturation are several. Considering the major problems related to abnormal sexual maturation we will discuss successively: (1) diagnosis of hypogonadotrophic hypogonadism in early infancy; (2) differential diagnosis between premature thelarche and true sexual precocity; (3) the usefulness of endocrine investigations in the evaluation of hypothalamic-pituitary function; and (4) the new developments in the treatment of precocious puberty, delayed puberty or hypogonadism.

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Gonadotropin‐releasing hormone release from the mediobasal hypothalamus of fetal baboons

Meyer

Pepe

1988

American J Primatol

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Pulsatile luteinizing-hormone releasing hormone (LHRH) secretion was measured from the mediobasal-suprachiasmatic-preoptic WBH-SCN-POA) region of the hypothalamus from fetal baboons (Pupw unubis) at midgestation (day 100; term = day 184). The entire MBH-SCN-POA (48 +_ 5 mg) was obtained between 1100 and 1200 hours and was immediately placed in icecold phosphate buffer (pH 7.4). The MBH-SCN-POA units were halved at the midline and superfused in parallel at 37.5"C for 5 hours. Then 500 pl of superfusate was collected at 10-minute intervals, and LHRH concentration was measured by radioimmunoassay using the Chen Ramirez antibody. In fetuses of untreated baboons (N = 3), LHRH pulse amplitude (mean +_ SE) was 16.0 f 4.2 pg, with a period of 30 f 1 minute; the average 10-minute output of LHRH was 9.4 f 2.0 pg. In fetal baboons in which the hormonal milieu in the mother was modulated by androstenedione treatment of midpregnancy (N = 3), average LHRH pulse amplitude was 1.7 * 0.3 pg, with a period of 33.5 f 4.9 minutes; the average 10-minute output of LHRH was 1.2 5 0.2 pg. Collectively, these data suggest that as early as midgestation, fetal baboons secrete LHRH in vitro in a pulsatile fashion and with a periodicity of 30-35 minutes. In addition, the decrease in LHRH pulse amplitude and the average 10-minute LHRH output (P < .01, P < .05) in tissue from fetal baboons of mothers in which the normal pattern of steroidogenesis is altered suggest that the output of LHRH systems in the fetus is sensitive to changes in the maternal hormonal milieu.

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Presence and activity of LH-RH in the mid-term human fetus

Cited by 14 publications

References 6 publications

G protein-coupled receptor expression in the adult and fetal adrenal glands

G protein-coupled receptor expression in the adult and fetal adrenal glands

Sexual maturation of the hypothalamus: Pathophysiological aspects and clinical implications

Gonadotropin‐releasing hormone release from the mediobasal hypothalamus of fetal baboons

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