Role of Ovarian Inhibin (Folliculostatin) in Regulating FSH Secretion in the Female Rat

Schwartz, Neena B.

doi:10.1007/978-1-4615-9278-5_2

Cited by 11 publications

(5 citation statements)

References 47 publications

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“…1B), and the enhancement or suppression of LH at one dose of pFF and GnRH in experiment 3 ( fig. 5C, F) are reminiscent of other occasional reports of LH enhancement or suppression with pFF in vivo [1,10,14,21,23,27], The lack of consistent findings, and the generally high dose of FF necessary to elicit LH changes, suggest that the LH effect is independent of the FSH effect. This impression is supported by in vitro studies.…”

Section: Discussionmentioning

confidence: 74%

“…In vitro, FF does not alter luteinizing hormone (LH) secretion under basal conditions: however, when cultures are challenged with gonadotropin releasing hormone (GnRH), LH secre tion may be suppressed or enhanced [8,16]. Most in vivo studies with FF demonstrate highly specific FSH suppres sion, with no alteration of LH [2,15,17,20], However, occasional reports of LH suppression [ 10,23,27] or enhance ment [1,14,21] after FF injection in vivo have provided confusing evidence regarding the specificity of FSH supReceived: May 13,1983 Accepted after revision: August 11,1983 pression by such fluid. When they occur, these effects on LH in vivo appear to be associated with the highest doses of FF and with high endogenous GnRH secretion [12], We and others have proposed that the FSH suppressing factor in FF named 'folliculostatin' or 'ovarian inhibin', is a hormone of the ovary which provides the crucial negative feedback signal which selectively maintains FSH levels low in the presence of ovaries.…”

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confidence: 99%

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Differential Suppression of FSH and LH Secretion by Follicular Fluid in the Presence or Absence of GnRH

Charlesworth¹,

Grady²,

Shin³

et al. 1984

Neuroendocrinology

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The differential role of porcine follicular fluid (pFF) in regulating follicle-stimulating hormone (FSH) and luteinizing hormone (LH) release in vivo in situations of different gonadotropin releasing hormone (GnRH) backgrounds was studied. In experiment 1, 2-week ovariectomized rats injected intravenously with 4, 16 or 64 mg of protein from pFF, showed a dose-dependent suppression of FSH over time, with a maximal suppression to 40% of control values by 10 h. LH levels were slightly, but significantly, elevated by the two lower doses, but not by the highest dose of pFF. In experiment 2,64 mg pFF was superimposed (i.v. injection) in ovariectomized rats injected subcutaneously with a high dose of GnRH antagonist (500 µg) 24 h earlier. The pFF suppressed FSH 35% below the level achieved in the absence of GnRH stimulation, with no effect on LH. In experiment 3, the rise in FSH secretion in acutely ovariectomized rats was shown to be inhibited by 8 or 32 mg pFF administered intravenously 3.5 h after surgery. Injection of GnRH (250 or 1,000 ng) 4.5 h after pFF could not overcome the inhibitory action of pFF on FSH, although non-pFF-treated controls responded in a dose-dependent fashion to GnRH stimulation. The expected LH response to GnRH was not affected by pFF, except in the group receiving 1,000 ng GnRH and 8 mg pFF. In these rats, LH was enhanced in one trial, but suppressed in a replicate trial, illustrating the inconsistent effects of pFF on LH under conditions of high GnRH stimulation. These results demonstrate the existence of a component of FSH secretion which is independent of GnRH, but sensitive to the inhibitory effect of pFF, suggesting a site of action of the putative peptide hormone, folliculostatin, distal to the GnRH receptor. Also, pFF always suppresses FSH (due to the action of folliculostatin); its effect on LH depends on the dose and the state of GnRH stimulation, and is probably not a function of folliculostatin per se.

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Section: Discussionmentioning

confidence: 74%

mentioning

confidence: 99%

Differential Suppression of FSH and LH Secretion by Follicular Fluid in the Presence or Absence of GnRH

Charlesworth¹,

Grady²,

Shin³

et al. 1984

Neuroendocrinology

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“…Initially, during the perinatal period, FSH induces Sertoli cell proliferation and establishes the final Sertoli cell number that will ultimately determine spermatogenic output, whereas later in development, FSH stimulates Sertoli cell transcriptional and metabolic activities, which contribute to the hormonal and nutritional environment necessary for germ cell survival and development [26][27][28][29][30][31][32][33][34][35]. In both males and females, FSH induces hormonal signals that return to the pituitary and hypothalamus as part of the feedback mechanism upholding the endocrine balance in the reproductive axis [36][37][38][39][40][41].…”

Section: The Gonadotropin Hormonesmentioning

confidence: 99%

Current Concepts of Follicle-Stimulating Hormone Receptor Gene Regulation1

George

Dille

Heckert

2011

Biology of Reproduction

110

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Follicle-stimulating hormone (FSH), a pituitary glycoprotein hormone, is an integral component of the endocrine axis that regulates gonadal function and fertility. To transmit its signal, FSH must bind to its receptor (FSHR) located on Sertoli cells of the testis and granulosa cells of the ovary. Thus, both the magnitude and the target of hormone response are controlled by mechanisms that determine FSHR levels and cell-specific expression, which are supported by transcription of its gene. The present review examines the status of FSHR/Fshr gene regulation, emphasizing the importance of distal sequences in FSHR/Fshr transcription, new insights gained from the influx of genomics data and bioinformatics, and emerging trends that offer direction in deciphering the FSHR/Fshr regulatory landscape.

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“…[1][2][3]. The well characterized and precisely timed increases in GnRH release (4) appears to represent an essential modulator of the preovulatory surge of LH and FSH on the day of proestrus (5)(6)(7), while the secondary estrous day surge of FSH is believed to be mainly regulated by a fall in inhibin (8)(9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Rapid Changes in the Expression of Inhibin α-, βA-, and βB-Subunits in Ovarian Cell Types During the Rat Estrous Cycle

Meunier¹,

Cajander²,

Roberts³

et al. 1988

Molecular Endocrinology

209

113

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Distributions of inhibin alpha-, beta A-, and beta B-subunits in different ovarian compartments were studied in cycling female rats by in situ hybridization with complementary RNA probes and using immunohistochemical localization with antibodies selective for each inhibin subunit. Consistent with earlier studies showing inhibin production by granulosa cells of maturing follicles, we also detected mRNAs for inhibin alpha-, beta A-, and beta B-subunits in granulosa cells of these follicles. However, based on immunohistochemistry and in situ hybridization, we found that inhibin alpha- is not only expressed in granulosa cells of mature follicles but in follicles at all stages of maturation, including primary to tertiary follicles. A number of primordial follicles also contained alpha mRNA and immunodetectable alpha-subunit. Interestingly, theca interna and interstitial gland cells contained inhibin alpha mRNA and alpha-subunit. Low levels of inhibin alpha immunoreactivity as well as specific hybridization to the complementary inhibin alpha mRNA probe were observed in newly formed luteal tissue. beta-Subunits, on the other hand, were detected exclusively in granulosa cells of healthy tertiary follicles. The changes in expression of inhibin alpha-, beta A-, and beta B-subunits were more pronounced during the follicular phase of the cycle: inhibin alpha reached its highest level in granulosa cells, theca interna, and interstitial gland cells a few hours after the LH/FSH surge, while at the same time the beta-subunits decreased dramatically in granulosa cells of mature follicles. Immediately before ovulation (estrus 0200 h), the alpha-subunit sharply declined in preovulatory follicles and was present mainly in granulosa cells from nonovulatory follicles at various stages of maturation. At that time, the beta A- and beta B-subunits could not be detected in preovulatory follicles but were localized mainly in small tertiary follicles (less than 300 microns). Unlike for the alpha- and beta B-subunits, beta A mRNA and immunoreactivity was present in large tertiary follicles (approximately 600 microns) immediately before ovulation. The present findings support the hypothesis that a decrease in inhibin production could be responsible for the secondary FSH surge observed early on estrus. This could be initiated by a change in the ratios of activin-inhibin production by decreasing first, the levels of beta-subunits, second, the levels of alpha-subunit, and third, by a resurgence of activin A produced mainly by granulosa cells from large tertiary follicles.(ABSTRACT TRUNCATED AT 400 WORDS)

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Role of Ovarian Inhibin (Folliculostatin) in Regulating FSH Secretion in the Female Rat

Cited by 11 publications

References 47 publications

Differential Suppression of FSH and LH Secretion by Follicular Fluid in the Presence or Absence of GnRH

Differential Suppression of FSH and LH Secretion by Follicular Fluid in the Presence or Absence of GnRH

Current Concepts of Follicle-Stimulating Hormone Receptor Gene Regulation1

Rapid Changes in the Expression of Inhibin α-, βA-, and βB-Subunits in Ovarian Cell Types During the Rat Estrous Cycle

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