Gonadotropin-releasing hormone, estradiol, and inhibin regulation of follicle-stimulating hormone and luteinizing hormone surges: Implications for follicle emergence and selection in heifers

James M. Haughian, O. J. Ginther, Francisco Javier Diaz, Milo C. Wiltbank

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Abstract

Mechanisms regulating gonadotropin surges and gonadotropin requirements for follicle emergence and selection were studied in heifers. Experiment 1 evaluated whether follicular inhibins regulate thepreovulatory luteinizing hormone (LH)/ follicle-stimulating hormone (FSH) surges elicited by gonadotropin- releasing hormone (GnRH) injection (Hour 1/4 0) and the subsequent periovulatory FSH surge. Treatments included control (n 1/4 6), steroid-depleted bovine follicular fluid (bFF) at Hour 4 (n 1/4 6), and bFF at Hour 6 (n 1/4 6). Gonadotropins in blood were assessed hourly from Hours 6 to 36, and follicle growth tracked by ultrasound. Consistent with inhibin independence, bFF at Hour 4 did not impact the GnRH-induced preovulatory FSH surge, whereas treatment at Hour 6 delayed onset of the periovulatory FSH surge and impeded growth of a new follicular wave. Experiment 2 examined GnRH and estradiol (E2) regulation of the periovulatory FSH surge. Treatment groups were control (n1/48), GnRH-receptor antagonist (GnRHr-ant, n1/4 8), and E2 + GnRHr-ant (n 1/4 4). GnRHr-ant (acyline) did not reduce the concentrations of FSH during the periovulatory surge and early follicle development (,7.0 mm) was unaffected, although subsequent growth of a dominant follicle (.8.0 mm) was prevented by GnRHr-ant. Addition of E2 delayed both the onset of the periovulatory FSH surge and emergence of a follicular wave. Failure to select a dominant follicle in the GnRHr-ant group was associated with reduced concentrations of LH but not FSH. Maximum diameter of F1 in controls (13.3 6 0.5 mm) was greater than in both GnRHr-ant(7.7 6 0.3 mm) and E2 + GnRHr-ant (6.7 6 0.8 mm) groups. Results indicated that the periovulatory FSHsurge stems from removal of negative stimuli (follicular E2 and inhibin), but is independent of GnRH stimulation. Emergence and early growth of follicles (until about 8 mm) requires the periovulatory FSH surge but not LH pulses. However, follicular deviation and late-stage growth of a single dominant follicle requires GnRH-dependent LH pulses.

Original languageEnglish (US)
Article number165
JournalBiology of reproduction
Volume88
Issue number6
DOIs
StatePublished - Aug 23 2013

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Inhibins
Follicle Stimulating Hormone
Luteinizing Hormone
Gonadotropin-Releasing Hormone
Ants
Estradiol
Follicular Fluid
Gonadotropins
Growth
LHRH Receptors
Hormone Antagonists
Therapeutics
Steroids
Control Groups
Injections

All Science Journal Classification (ASJC) codes

  • Reproductive Medicine
  • Cell Biology

Cite this

@article{b4ef5871d59243bdbcbc7a6600d57889,
title = "Gonadotropin-releasing hormone, estradiol, and inhibin regulation of follicle-stimulating hormone and luteinizing hormone surges: Implications for follicle emergence and selection in heifers",
abstract = "Mechanisms regulating gonadotropin surges and gonadotropin requirements for follicle emergence and selection were studied in heifers. Experiment 1 evaluated whether follicular inhibins regulate thepreovulatory luteinizing hormone (LH)/ follicle-stimulating hormone (FSH) surges elicited by gonadotropin- releasing hormone (GnRH) injection (Hour 1/4 0) and the subsequent periovulatory FSH surge. Treatments included control (n 1/4 6), steroid-depleted bovine follicular fluid (bFF) at Hour 4 (n 1/4 6), and bFF at Hour 6 (n 1/4 6). Gonadotropins in blood were assessed hourly from Hours 6 to 36, and follicle growth tracked by ultrasound. Consistent with inhibin independence, bFF at Hour 4 did not impact the GnRH-induced preovulatory FSH surge, whereas treatment at Hour 6 delayed onset of the periovulatory FSH surge and impeded growth of a new follicular wave. Experiment 2 examined GnRH and estradiol (E2) regulation of the periovulatory FSH surge. Treatment groups were control (n1/48), GnRH-receptor antagonist (GnRHr-ant, n1/4 8), and E2 + GnRHr-ant (n 1/4 4). GnRHr-ant (acyline) did not reduce the concentrations of FSH during the periovulatory surge and early follicle development (,7.0 mm) was unaffected, although subsequent growth of a dominant follicle (.8.0 mm) was prevented by GnRHr-ant. Addition of E2 delayed both the onset of the periovulatory FSH surge and emergence of a follicular wave. Failure to select a dominant follicle in the GnRHr-ant group was associated with reduced concentrations of LH but not FSH. Maximum diameter of F1 in controls (13.3 6 0.5 mm) was greater than in both GnRHr-ant(7.7 6 0.3 mm) and E2 + GnRHr-ant (6.7 6 0.8 mm) groups. Results indicated that the periovulatory FSHsurge stems from removal of negative stimuli (follicular E2 and inhibin), but is independent of GnRH stimulation. Emergence and early growth of follicles (until about 8 mm) requires the periovulatory FSH surge but not LH pulses. However, follicular deviation and late-stage growth of a single dominant follicle requires GnRH-dependent LH pulses.",
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year = "2013",
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T1 - Gonadotropin-releasing hormone, estradiol, and inhibin regulation of follicle-stimulating hormone and luteinizing hormone surges

T2 - Implications for follicle emergence and selection in heifers

AU - Haughian, James M.

AU - Ginther, O. J.

AU - Diaz, Francisco Javier

AU - Wiltbank, Milo C.

PY - 2013/8/23

Y1 - 2013/8/23

N2 - Mechanisms regulating gonadotropin surges and gonadotropin requirements for follicle emergence and selection were studied in heifers. Experiment 1 evaluated whether follicular inhibins regulate thepreovulatory luteinizing hormone (LH)/ follicle-stimulating hormone (FSH) surges elicited by gonadotropin- releasing hormone (GnRH) injection (Hour 1/4 0) and the subsequent periovulatory FSH surge. Treatments included control (n 1/4 6), steroid-depleted bovine follicular fluid (bFF) at Hour 4 (n 1/4 6), and bFF at Hour 6 (n 1/4 6). Gonadotropins in blood were assessed hourly from Hours 6 to 36, and follicle growth tracked by ultrasound. Consistent with inhibin independence, bFF at Hour 4 did not impact the GnRH-induced preovulatory FSH surge, whereas treatment at Hour 6 delayed onset of the periovulatory FSH surge and impeded growth of a new follicular wave. Experiment 2 examined GnRH and estradiol (E2) regulation of the periovulatory FSH surge. Treatment groups were control (n1/48), GnRH-receptor antagonist (GnRHr-ant, n1/4 8), and E2 + GnRHr-ant (n 1/4 4). GnRHr-ant (acyline) did not reduce the concentrations of FSH during the periovulatory surge and early follicle development (,7.0 mm) was unaffected, although subsequent growth of a dominant follicle (.8.0 mm) was prevented by GnRHr-ant. Addition of E2 delayed both the onset of the periovulatory FSH surge and emergence of a follicular wave. Failure to select a dominant follicle in the GnRHr-ant group was associated with reduced concentrations of LH but not FSH. Maximum diameter of F1 in controls (13.3 6 0.5 mm) was greater than in both GnRHr-ant(7.7 6 0.3 mm) and E2 + GnRHr-ant (6.7 6 0.8 mm) groups. Results indicated that the periovulatory FSHsurge stems from removal of negative stimuli (follicular E2 and inhibin), but is independent of GnRH stimulation. Emergence and early growth of follicles (until about 8 mm) requires the periovulatory FSH surge but not LH pulses. However, follicular deviation and late-stage growth of a single dominant follicle requires GnRH-dependent LH pulses.

AB - Mechanisms regulating gonadotropin surges and gonadotropin requirements for follicle emergence and selection were studied in heifers. Experiment 1 evaluated whether follicular inhibins regulate thepreovulatory luteinizing hormone (LH)/ follicle-stimulating hormone (FSH) surges elicited by gonadotropin- releasing hormone (GnRH) injection (Hour 1/4 0) and the subsequent periovulatory FSH surge. Treatments included control (n 1/4 6), steroid-depleted bovine follicular fluid (bFF) at Hour 4 (n 1/4 6), and bFF at Hour 6 (n 1/4 6). Gonadotropins in blood were assessed hourly from Hours 6 to 36, and follicle growth tracked by ultrasound. Consistent with inhibin independence, bFF at Hour 4 did not impact the GnRH-induced preovulatory FSH surge, whereas treatment at Hour 6 delayed onset of the periovulatory FSH surge and impeded growth of a new follicular wave. Experiment 2 examined GnRH and estradiol (E2) regulation of the periovulatory FSH surge. Treatment groups were control (n1/48), GnRH-receptor antagonist (GnRHr-ant, n1/4 8), and E2 + GnRHr-ant (n 1/4 4). GnRHr-ant (acyline) did not reduce the concentrations of FSH during the periovulatory surge and early follicle development (,7.0 mm) was unaffected, although subsequent growth of a dominant follicle (.8.0 mm) was prevented by GnRHr-ant. Addition of E2 delayed both the onset of the periovulatory FSH surge and emergence of a follicular wave. Failure to select a dominant follicle in the GnRHr-ant group was associated with reduced concentrations of LH but not FSH. Maximum diameter of F1 in controls (13.3 6 0.5 mm) was greater than in both GnRHr-ant(7.7 6 0.3 mm) and E2 + GnRHr-ant (6.7 6 0.8 mm) groups. Results indicated that the periovulatory FSHsurge stems from removal of negative stimuli (follicular E2 and inhibin), but is independent of GnRH stimulation. Emergence and early growth of follicles (until about 8 mm) requires the periovulatory FSH surge but not LH pulses. However, follicular deviation and late-stage growth of a single dominant follicle requires GnRH-dependent LH pulses.

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U2 - 10.1095/biolreprod.112.107342

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