Effects of the gonadotropin-releasing hormone associated peptides (GAP) on the release of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) in vivo

Yu, Wen H.; Arisawa, Masayoshi; Millar, Robert P.; McCann, Samuel M.

doi:10.1016/0196-9781(89)90004-1

Cited by 13 publications

(5 citation statements)

References 9 publications

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“…These findings indicate that NPY can be involved in the modulation of LH and FSH release in opposite ways and are consistent with a separate hypo thalamic control of FSH release [16].…”

Section: Discussionsupporting

confidence: 71%

Effects of Neuropeptide Y on Gonadotropin and Prolactin Release in Normal, Castrated or Flutamide-Treated Male Rats

Reznikov

McCann

1993

Neuroendocrinology

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This study was carried out to clarify the central effects of neuropeptide Y (NPY) on gonadotropin and prolactin (PRL) release in the male rat and to evaluate the hypothesis that it may play a role in negative feedback regulation of gonadotropin secretion in the male. NPY (4 µg in 2 µl 0.9% NaCl) or an equal volume of saline was microinjected into the third cerebral ventricle of conscious, unrestrained rats and its effects on plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH) and PRL cencentrations, and the gonadotropin response to LH-releasing hormone (LHRH) were measured by radioimmunoassay in noncastrated, castrated (3 days before the experiment) rats or animals treated with flutamide, an androgen receptor blocker (10 mg/kg b.w. per day subcutaneously for 3 days). Blood samples were drawn periodically from a Silastic catheter in the external jugular vein just before and for 120 min after intraventricular injections. At 90 min after injection 25 ng of LHRH were infused intravenously and 3 additional blood samples were withdrawn at 10-min intervals after the injection. Normal male rats responded to NPY with a decrease in plasma LH concentrations at 60 min. Plasma LH was significantly lower at 120 min than values in the saline-injected controls. At that time there was a significant 2-fold augmentation of their response to LHRH. In contrast, NPY elevated plasma FSH significantly versus values in controls at 15 and 30 min after injection, but the FSH release in response to LHRH was not altered. In castrated males NPY caused a rapid decline of their elevated plasma LH levels. At 60 min after NPY injection the mean plasma LH concentration was 22% of the initial level; meanwhile, plasma FSH levels were not significantly changed. The castrates displayed no change in LH responsiveness to LHRH as compared to the response of saline-injected control rats, but had a highly significant increase in FSH responsiveness. In flutamide-treated animals which had slightly elevated initial plasma LH values, NPY altered the plasma LH concentrations in a similar manner to those of normal rats; however, there was a decreased response to LHRH, and plasma FSH and responsiveness of FSH to LHRH were unaltered. At 30 min after NPY injection PRL levels decreased significantly in all experimental groups and remained low for the duration of the experiment. The mean area under the plasma PRL concentration curves for the 2-hour duration of the experiment relative to the control values was 44% in normal rats and 64% in the castrates. The results of this work demonstrate the suppressive effect of this dose of NPY injected into the third cerebral ventricle on LH and PRL release which was accompanied by a sensitization of the response of LH to LHRH in normal rats only and an increase in plasma FSH in normals and an increased response of FSH to LHRH in castrate animals only. Because NPY mimics the action of androgens on LHRH release, we suggest that it may be involved in negative feedback regulation of LHRH release in male rats.

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“…These findings indicate that NPY can be involved in the modulation of LH and FSH release in opposite ways and are consistent with a separate hypo thalamic control of FSH release [16].…”

Section: Discussionsupporting

confidence: 71%

Effects of Neuropeptide Y on Gonadotropin and Prolactin Release in Normal, Castrated or Flutamide-Treated Male Rats

Reznikov

McCann

1993

Neuroendocrinology

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“…Nikolics et al reported in 1985 that GAP is an inhibitor of prolactin release and that administration of neutralizing antibodies against GAP to rabbits causes elevation of serum prolactin (Nikolics et al, 1985). Some groups have reported similar results (Chavali et al, 1997; Milton et al, 1992), while other groups have been unable to replicate these findings (Chandrashekar et al, 1988; Ishibashi et al, 1987; Pohl et al, 1988; Thomas et al, 1988; Yu et al, 1989). These findings prompted Moretuzzo et al (1992) to screen for GNRH1 deletions by Southern blotting in patients with hyperprolactinemia; they identified no gross changes in 15 patients.…”

Section: The Search For Gnrh1mutations In Ihhmentioning

confidence: 97%

A needle in a haystack: Mutations in GNRH1 as a rare cause of isolated GnRH deficiency

Chan

2011

Molecular and Cellular Endocrinology

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GNRH1, the human gene that gives rise to GnRH, has long been an obvious candidate gene for idiopathic hypogonadotropic hypogonadism, particularly because the hpg mouse, a mouse model of isolated hypogonadotropic hypogonadism, carries a deletion that disrupts Gnrh1. In 2009, 25 years after the sequence of human GNRH1 was initially determined, two groups independently reported homozygous frameshift mutations in GNRH1 in patients with idiopathic hypogonadotropic hypogonadism. In two additional families, heterozygous GNRH1 mutations segregated with idiopathic hypogonadotropic hypogonadism. In the first family, the mutation occurred alone in four female subjects, whereas in the second it co-existed with a mutation in NR0B1/DAX1 to cause delayed puberty in two female subjects. While hemizygous mutations the X-linked NR0B1 are a well-known cause of hypogonadotropic hypogonadism and adrenal hypoplasia in male patients, heterozygous female carriers are generally asymptomatic. Thus, mutations in GNRH1 have been associated with both mild and severe forms of GnRH deficiency, and may work in combination with other gene mutations to produce GnRH-deficient phenotypes.

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“…GAP seems to be a releasing factor for gonadotrophins in rats Yu et al, 1988;Kerrigan et al, 1995). There is some evidence of separation of neuroendocrine effects within the molecule (Millar et al, 1986), since GAP(1-13), more effective in stimulating gonadotrophin release, exerts a preferential follicle-stimulating hormone-releasing activity (Yu et al, 1989). Moreover, it has been found in vitro and in vivo, that GAP possess strong prolactininhibiting properties in rats and humans Yu et al, 1988;Wormald et al, 1989;Vacher et al, 1991).…”

Section: Introductionmentioning

confidence: 97%

“…However, its hypophysiotrophic functions in sheep are puzzling (Thomas et al, 1988) and the physiological role in mammals are still not understood. According to Culler and Negro-Villar (1986), studies of proGnRH processing during various physiologic states will greatly advance our understanding of the neuroendocrine control of reproduction, particularly if the non-GnRH portion of the molecule contains additional biologically active peptides Millar et al, 1986;Yu et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Gonadotrophin-releasing hormone and GnRH-associated peptide neurobiology from the rearing period until puberty in the female sheep

Wańkowska¹,

Polkowska²

2009

Journal of Chemical Neuroanatomy

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Effects of the gonadotropin-releasing hormone associated peptides (GAP) on the release of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) in vivo

Cited by 13 publications

References 9 publications

Effects of Neuropeptide Y on Gonadotropin and Prolactin Release in Normal, Castrated or Flutamide-Treated Male Rats

Effects of Neuropeptide Y on Gonadotropin and Prolactin Release in Normal, Castrated or Flutamide-Treated Male Rats

A needle in a haystack: Mutations in GNRH1 as a rare cause of isolated GnRH deficiency

Gonadotrophin-releasing hormone and GnRH-associated peptide neurobiology from the rearing period until puberty in the female sheep

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