Regulation of Luteinizing-Hormone-Receptors and Steroidogenesis in the Neonatal Rat Testis

Huhtaniemi, Ilpo; Katikineni, Mohan; Catt, Kevin J.

doi:10.1210/endo-109-2-588

Cited by 83 publications

(49 citation statements)

References 28 publications

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“…Prolactin administration begun immediately after hypophysectomy mitigates the loss of LH receptors but does not prevent the loss of the testis ability to secrete testosterone after LH stimulation (Zipf et al, 1978a). Thus our results suggest testosterone secretion is not a requirement and is more consistent with the suggestion that LH induction of LH receptors is due to general changes in membrane conformation leading to exposure of cryptic membrane receptors (Baranao and Dufau, 1983;Huhtaniemi et al, 1981).…”

Section: Discussionsupporting

confidence: 82%

Temporal relationship of the prolactin‐dependent LH‐induced LH receptor to the LH stimulus

Hussein

Zipf

1988

Journal Cellular Physiology

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The time course for LH induction of luteinizing hormone (LH) receptors as reflected in binding of 125I-labeled hCG was investigated in hypophysectomized adult male rats. A low dose of oLH (10 micrograms) was administered to hypophysectomized adult male rats following pretreatments with prolactin, follicle-stimulating hormone (FSH), growth hormone (GH), or saline. Testicular binding of hCG was determined at different times following the LH injection using Leydig cell membrane preparations from a testicular homogenate. Seven days after hypophysectomy, hCG binding was at a nadir of 19 +/- 7% (mean +/- SD) of control values. Pretreatment with prolactin (100 micrograms/day) for 7 days was associated with a nonsignificantly different hCG binding that was 30 +/- 5% of control values. Prolactin pretreatment plus a single 10 micrograms LH i.p. injection increased 125I hCG binding up to 56 +/- 10% of control values within 30 minutes of the LH injection. Luteinizing hormone-induced hCG binding persisted at a high level (51 +/- 4% of control values) for 2 hours but returned to hypophysectomized control levels 6 hours after the i.p. LH injection. Seven days pretreatment with FSH or GH at 100 micrograms/day plus 10-micrograms LH injections was also tested. Neither FSH nor GH had a statistically significant effect on hCG binding nor could they mimic the ability of prolactin to allow for LH induction of hCG binding in the hypophysectomized adult male rats. These studies suggest that the induction or "up-regulation" of Leydig cell hCG binding by ovine LH is rapid and specifically dependent upon pre-exposure to prolactin.

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Section: Discussionsupporting

confidence: 82%

Temporal relationship of the prolactin‐dependent LH‐induced LH receptor to the LH stimulus

Hussein

Zipf

1988

Journal Cellular Physiology

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“…The stimulatory effect of hCG that rapidly increases [Ca 2ϩ ] i is responsible at least in part for the regulation of SF-1-mediated StAR expression that consequently regulates steroidogenesis in mouse Leydig tumor cells. (Endocrinology 140: 1739 -1751, 1999) T HE ENDOCRINE regulation of Leydig cells occurs predominantly through the LH/hCG receptor after coupling to the adenylate cyclase signal transduction system (1,2). The role of Ca 2ϩ as a second messenger has been extensively studied in the regulation of diverse cellular functions (3)(4)(5).…”

Section: Camentioning

confidence: 99%

Functional Assessment of the Calcium Messenger System in Cultured Mouse Leydig Tumor Cells: Regulation of Human Chorionic Gonadotropin-Induced Expression of the Steroidogenic Acute Regulatory Protein

Manna¹

1999

Endocrinology

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The steroidogenic acute regulatory (StAR) protein, a 30-kDa mitochondrial factor, is a key regulator of steroid hormone biosynthesis, facilitating the transfer of cholesterol from the outer to the inner mitochondrial membrane. StAR protein expression is restricted to steroidogenic tissues, and it responds to hormonal stimulation through different second messenger pathways. The present study was designed to explore the mechanisms of extracellular calcium (Ca 2ϩ

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“…androgen biosynthesis, spermatogenesis and Leydig cell morphology. Huhtaniemi et al (1981b), Huhtaniemi, Nozu, Warren, Dufau & Catt (1982) and (Tähkä, 1978). They still retain, however, certain features considered specific for Leydig cells, i.e.…”

Section: Introductionmentioning

confidence: 99%

Photoperiodic modulation of testicular LH receptors in the bank vole (Clethrionomys glareolus)

Tähkä¹,

Rajaniemi²

1985

Reproduction

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Regulation of Luteinizing-Hormone-Receptors and Steroidogenesis in the Neonatal Rat Testis

Cited by 83 publications

References 28 publications

Temporal relationship of the prolactin‐dependent LH‐induced LH receptor to the LH stimulus

Temporal relationship of the prolactin‐dependent LH‐induced LH receptor to the LH stimulus

Functional Assessment of the Calcium Messenger System in Cultured Mouse Leydig Tumor Cells: Regulation of Human Chorionic Gonadotropin-Induced Expression of the Steroidogenic Acute Regulatory Protein

Photoperiodic modulation of testicular LH receptors in the bank vole (Clethrionomys glareolus)

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