Leydig cell receptors for luteinizing hormone releasing hormone and its agonists and their modulation by administration or deprivation of the releasing hormone

Sharpe, Richard M.; Fraser, Hamish M.

doi:10.1016/0006-291x(80)90732-9

Cited by 132 publications

(39 citation statements)

References 16 publications

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“…The presence of GnRH receptors in Leydig cells (Clayton et al 1980, Sharpe & Fraser 1980a and in granulosa and luteal cells (Clayton et al 1979, Harwood et al 1980a,b, Reeves et al 1980 has been supported by the identification of a mRNA with a sequence identical to that of the pituitary GnRH-R (Moumni et al 1994). However, the exact nature of the endogenous GnRH-like material found in Sertoli cells (Sharpe & Fraser 1980b, Paull et al 1981, Bhasin et al 1983 and in granulosa cells (Aten et al 1986) of adult rats remains uncertain.…”

Section: Discussionmentioning

confidence: 98%

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Fetal expression of GnRH and GnRH receptor genes in rat testis and ovary

Botte

Chamagne²,

Carre³

et al. 1998

Journal of Endocrinology

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The identification of gonadal gonadotropin-releasing hormone receptors (GnRH-R) and evidence of direct inhibitory effects of GnRH agonists upon steroidogenesis in adult rat gonads, lend credence to a putative intragonadal role of a locally secreted GnRH or GnRH-like peptide. Using reverse transcription-polymerase chain reaction followed by Southern blot hybridization and sequencing, we identified, both in the ovary and in the testis of fetal and adult rats, a fully processed GnRH messenger RNA (mRNA), the sequence of which, in adult testis, was identical to that found in the hypothalamus. We also detected in the testis, but not in the ovary, a transcript containing the first intron.The ontogeny of GnRH and GnRH-R gene expression was studied in rat gonads from 14·5 to 21·5 days postcoitum (dpc), using dot blot hybridization of total RNA. During this period, the levels of cyclophilin mRNA normalized to total RNA remained unchanged. Thus, we used cyclophilin as an internal standard. GnRH mRNA was detected in the ovary at 18·5 dpc, four days later than in the testis, and similar levels were found in both sexes at birth. GnRH-R mRNA was present at 14·5 dpc in the testis and at 15·5 dpc in the ovary, with the levels at 21·5 dpc being 2·4 times higher in the testis than in the ovary. GnRH and GnRH-R mRNA levels increased in both sexes in late fetal development, but this increase appeared two days sooner in the ovary compared with the testis, thus supporting the hypothesis that expression of the GnRH and GnRH-R genes is regulated in a sexdependent manner during fetal development. In all cases, expression of GnRH and GnRH-R preceded gonadotropin receptors in the gonads and initiation of gonadotropin secretion by the pituitary.

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Section: Discussionmentioning

confidence: 98%

“…Radioligand binding assays first demonstrated their existence on Leydig cells (Clayton et al 1980, Sharpe & Fraser 1980a) and on granulosa and luteal cells (Clayton et al 1979, Harwood et al 1980a,b, Reeves et al 1980. We have shown that the primary structure of this gonadal GnRH-R is identical to the pituitary one (Moumni et al 1994).…”

Section: Introductionmentioning

confidence: 99%

Fetal expression of GnRH and GnRH receptor genes in rat testis and ovary

Botte

Chamagne²,

Carre³

et al. 1998

Journal of Endocrinology

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“…Rat Leydig cells contain high-affinity receptors for GnRH. 37 In regard to the events that occur downstream of GnRH signalling, the stimulatory effect of GnRH has been shown to be independent on the cAMP-protein kinase system. However, this effect is calcium-dependent [2][3][4] and involves protein kinase C in rat Leydig cells.…”

Section: Gnrh Regulates Steroidogenesis In Rat Leydig Cells B Yao Et mentioning

confidence: 99%

Gonadotropin-releasing hormone positively regulates steroidogenesis via extracellular signal-regulated kinase in rat Leydig cells

Yao

Liu²,

Gu³

et al. 2011

Asian J Androl

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Gonadotropin-releasing hormone (GnRH) is secreted from neurons within the hypothalamus and is necessary for reproductive function in all vertebrates. GnRH is also found in organs outside of the brain and plays an important role in Leydig cell steroidogenesis in the testis. However, the signalling pathways mediating this function remain largely unknown. In this study, we investigated whether components of the mitogen-activated protein kinase (MAPK) pathways are involved in GnRH agonist (GnRHa)-induced testis steroidogenesis in rat Leydig cells. Primary cultures of rat Leydig cells were established. The expression of 3b-hydroxysteroid dehydrogenase (3b-HSD) and the production of testosterone in response to GnRHa were examined at different doses and for different durations by RT-PCR, Western blot analysis and radioimmunoassay (RIA). The effects of GnRHa on ERK1/2, JNK and p38 kinase activation were also investigated in the presence or absence of the MAPK inhibitor PD-98059 by Western blot analysis. GnRHa induced testosterone production and upregulated 3b-HSD expression at both the mRNA and protein levels; it also activated ERK1/2, but not JNK and p38 kinase. Although the maximum effects of GnRHa were observed at a concentration of 100 nmnol L 21 after 24 h, activation of ERK1/2 by GnRHa reached peak at 5 min and it returned to the basal level within 60 min. PD-98059 completely blocked the activation of ERK1/2, the upregulation of 3b-HSD and testosterone production. Our data show that GnRH positively regulates steroidogenesis via ERK signalling in rat Leydig cells. ERK1/2 activation by GnRH may be responsible for the induction of 3b-HSD gene expression and enzyme production, which may ultimately modulate steroidogenesis in rat Leydig cells.

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“…Similar changes have also been observed in GnRH-immunized marmoset monkeys (Hodges & Hearn, 1977) and rhesus monkeys (Chappel, Ellinwood, Huckins, Herbert & Spies, 1980). Because the inhibitory effects of the immunization are so severe, its use as a contraceptive in man has not been considered but there is potential in the veterinary field for a non-surgical method of castration, particularly in meat production (Fraser, 1980a;Short, 1980;Robertson, Wilson, Rowland & Fraser, 1981 (Rivier, Rivier & Vale, 1980 (Rivier et al, 1980). Possible direct action of antagonists on the testes remains to be established.…”

Section: Gnrh Antibodiesmentioning

confidence: 70%

Antifertility effects of GnRH

Fraser¹

1982

Reproduction

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Leydig cell receptors for luteinizing hormone releasing hormone and its agonists and their modulation by administration or deprivation of the releasing hormone

Cited by 132 publications

References 16 publications

Fetal expression of GnRH and GnRH receptor genes in rat testis and ovary

Fetal expression of GnRH and GnRH receptor genes in rat testis and ovary

Gonadotropin-releasing hormone positively regulates steroidogenesis via extracellular signal-regulated kinase in rat Leydig cells

Antifertility effects of GnRH

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