Regulation of somatostatin and growth hormone-releasing factor by gonadal steroids in fetal rat hypothalamic cells in culture

Fernandez, G.; Sánchez‐Franco, Franco; Frailes, Maria Teresa de los; Tolón, Rosa M.; Lorenzo, María Jesús López; López, J. Villalón; Cacicedo, Lucinda

doi:10.1016/0167-0115(92)90093-a

Cited by 18 publications

(5 citation statements)

References 34 publications

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“…In humans, the primary action of the sex steroids on GH release appears to occur at the level of the somatostatic neurons, and the steroids could modulate the production of somatostatin by affecting α 2 -adrenergic pathways (Devesa et al 1991(Devesa et al , 1992. In cultured fetal rat hypothalamic cells, testosterone inhibits somatostatin production and stimulates the effect of GHRH (Fernandez et al 1992). These results were supported by Ono and Miki (1989), who reported that somatostatin release from cultured hypothalamic rat cells increases in castrated rats.…”

Section: Discussionsupporting

confidence: 56%

“…For example, in static cultures of bovine anterior pituitary cells androgens have been demonstrated to increase the responsiveness of these cells to GHRH (Hassan et al 1992). There is also evidence that both somatostatin and GHRH are influenced by testosterone and estradiol at the level of the hypothalamus (Fernandez et al 1992). In humans, while testosterone stimulates the secretion of somatostatin, 17β-estradiol inhibits the secretion of this hormone (Devesa et al 1991).…”

Section: Introductionmentioning

confidence: 97%

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Effect of testosterone on growth hormone gene expression in the goldfish pituitary

Huggard¹,

Khakoo²,

Kassam³

et al. 1996

Can. J. Physiol. Pharmacol.

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This study investigated the effects of testosterone and a nonaromatizable androgen, 11 beta-hydroxyandrosterone, on growth hormone gene expression in the goldfish pituitary. In the sexually immature goldfish, treatment with physiological doses of both testosterone and 11 beta-hydroxyandrosterone significantly increased the growth hormone mRNA production above basal levels. However, at supraphysiological doses, treatment with these androgens resulted in a lower level of stimulation or an inhibition of growth hormone mRNA levels. In sexually mature goldfish, testosterone treatment stimulated growth hormone mRNA levels in a dose-related fashion, with a lower level of sensitivity compared with sexually immature fish. To investigate the direct action of testosterone at the level of the pituitary, studies were performed in vitro, using isolated pituitaries obtained from both sexually immature and mature goldfish. A dose-dependent stimulation of the pituitary growth hormone mRNA level was observed in both sexually immature and mature goldfish. Overall, the present results indicate that physiological concentrations of androgens stimulate pituitary growth hormone synthesis in both sexually immature and mature goldfish. The observed stimulatory effect of testosterone occurs directly at the level of the pituitary, although it is possible that testosterone may also exert indirect effects through other neuroendocrine factors.

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Section: Discussionsupporting

confidence: 56%

Section: Introductionmentioning

confidence: 97%

Effect of testosterone on growth hormone gene expression in the goldfish pituitary

Huggard¹,

Khakoo²,

Kassam³

et al. 1996

Can. J. Physiol. Pharmacol.

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“…Quintela et al (1997b) Dual Glucocorticoids In vivo injection induced while in vitro hypothalamic segment perfusion decreased SRIF secretion Estupina et al (1997) a All experiments were carrried out in male rats. b Some report decreased somatostatin level following sex steroid treatment (Fernandez et al 1992, Hassan et al 2001. This discrepance may be due to the experimental approach including whether treatment was conducted in vivo or in vitro, treatment duration and dose, sex of the animal model and species.…”

Section: Ion Channel Regulationmentioning

confidence: 99%

Somatostatin system: molecular mechanisms regulating anterior pituitary hormones

Eigler¹,

Ben-Shlomo²

2014

Journal of Molecular Endocrinology

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The somatostatin (SRIF) system, which includes the SRIF ligand and receptors, regulates anterior pituitary gland function, mainly inhibiting hormone secretion and to some extent pituitary tumor cell growth. SRIF-14 via its cognate G-protein-coupled receptors (subtypes 1-5) activates multiple cellular signaling pathways including adenylate cyclase/cAMP, MAPK, ion channel-dependent pathways, and others. In addition, recent data have suggested SRIF-independent constitutive SRIF receptor activity responsible for GH and ACTH inhibition in vitro. This review summarizes current knowledge on ligand-dependent and independent SRIF receptor molecular and functional effects on hormone-secreting cells in the anterior pituitary gland.

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“…Anterior pituitaries were separated from the neurohypophysis. The brain was dissected from the hypothalamus as previously described [15]. Pituitaries and hypothalami were divided into two halves for peptide extraction and RNA isolation.…”

Section: Methodsmentioning

confidence: 99%

“…Peptide extraction was performed as previously described [15], and samples were stored at –20°C until assayed for IR-SRIH, IR-GHRH, IR-GH, IR-LH and IR-FSH content. Protein recovery was between 90–100%, as previously described [16].…”

Section: Methodsmentioning

confidence: 99%

Regulation of Gonadal and Somatotropic Axis by Chronic Intraventricular Infusion of Insulin-Like Growth Factor 1 Antibody at the Initiation of Puberty in Male Rats

Pazos

Sánchez‐Franco²,

Balsa³

et al. 1999

Neuroendocrinology

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There has been increasing experimental evidence to suggest that insulin-like growth factor 1 (IGF-I) may be one of the essential regulators in the reproductive system of the rat. IGF-I is synthesized in the hypothalamus and IGF-I immunoreactivity increases during puberty. Consequently we hypothesized that centrally located IGF-I might contribute to the initiation of puberty. Centrally located IGF-I was immunoneutralized to assess this hypothesis. Male Wistar rats, 28 days old, were infused intracerebroventricularly with specific purified IgGs from rabbit IGF-I antiserum (IGF-I-Ab). The intracerebroventricular administration of IGF-I-Ab resulted in a reduction in testicular weight and consequently in delayed pubertal development. There was also a reduction in serum testosterone, pituitary immunoreactive (IR) luteinizing hormone (LH) and serum IR follicle-stimulating hormone (FSH). The accumulation of βLH mRNA was not modified, whereas βFSH mRNA was increased. An increment in the serum growth hormone (GH) levels was also observed. There were no significant alterations in hypothalamic IR growth hormone releasing factor content, although IR somatostatin (SRIH) content was increased by IGF-I-Ab. The body weight gain remained unaltered. As a whole, our study suggests that centrally located IGF-I influences pubertal development, production and release of gonadotropins and supports the finding that endogenous centrally located IGF-I plays a role at the initiation of puberty in the male rat. It also gives support to the physiological role of centrally located IGF-I in the release of GH mediated by hypothalamic SRIH at the initiation of puberty.

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Regulation of somatostatin and growth hormone-releasing factor by gonadal steroids in fetal rat hypothalamic cells in culture

Cited by 18 publications

References 34 publications

Effect of testosterone on growth hormone gene expression in the goldfish pituitary

Effect of testosterone on growth hormone gene expression in the goldfish pituitary

Somatostatin system: molecular mechanisms regulating anterior pituitary hormones

Regulation of Gonadal and Somatotropic Axis by Chronic Intraventricular Infusion of Insulin-Like Growth Factor 1 Antibody at the Initiation of Puberty in Male Rats

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