Neuroendocrine vs. Paracrine Control of Follicle-Stimulating Hormone

Padmanabhan, Vasantha; Sharma, Tejinder Pal

doi:10.1016/s0188-4409(01)00318-6

Cited by 33 publications

(29 citation statements)

References 126 publications

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“…Mean (n ϭ 6 per treatment group; one in each group exhibited an LH surge during the study and excluded from analyses for that period) concentrations of LH (top panel), LH pulse frequency (middle panel), and LH pulse amplitude (bottom panel) from control (Ⅺ) and prenatal T (f) females at 24 wk of age. Time points correspond to before GnRH-A administration (Pre), during GnRH-A administration, after cessation of GnRH-A administration (24,48, and 72 h post-GnRH A), and during E 2 treatment (E 2 ). See Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Time points correspond to before GnRH-A administration (Pre), during GnRH-A administration, after cessation of GnRH-A administration (24,48, and 72 h), and during E 2 treatment. See Fig.…”

Section: Fig 5 Mean (N ϭ 7 Per Treatment Group) Concentrations Of Lmentioning

confidence: 99%

“…4). Blood samples were taken at 10-min intervals for 6 h before GnRH-A administration (Pre), thrice after cessation of GnRH-A treatment (24,48, and 72 h), and during E 2 implant. See Fig.…”

Section: Age-associated Changes In E 2 Negative Feedbackmentioning

confidence: 99%

“…Considering that LH and FSH are produced by the same gonadotrope (42,43), and E 2 is a major negative feedback regulator of both LH and FSH at the pituitary level (23)(24)(25), one would expect changes in feedback sensitivity to E 2 be reflected by changes in circulating FSH. Although the reduced responsiveness to E 2 negative feedback was reflected as an increase in circulating LH concentrations and LH pulse frequency in the prenatal T females after GnRH-A and E 2 treatment, no such differences in circulating levels of FSH were evident in prenatal T females at either 12 or 24 wk.…”

Section: Differential Programming Of E 2 Feedback Control Of Lh and Fshmentioning

confidence: 99%

“…Our results indicate that this indeed is the case and further that development of hypergonadotropism occurs progressively over time. In addition, because E 2 , along with inhibin (23)(24)(25), is a major negative feedback regulator of FSH, the second hypothesis we tested is that the reduced sensitivity to E 2 feedback will also be reflected as increased FSH secretion in the prenatal T females. Our results indicate that this is not the case and leads to the conclusion that prenatal T treatment has differential effects on feedback responsiveness of LH and FSH to E 2 .…”

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confidence: 99%

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Fetal Programming: Excess Prenatal Testosterone Reduces Postnatal Luteinizing Hormone, But Not Follicle-Stimulating Hormone Responsiveness, to Estradiol Negative Feedback in the Female

Sarma¹,

Manikkam²,

Herkimer³

et al. 2005

Endocrinology

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Exposure of female sheep fetuses to excess testosterone (T) during early to midgestation produces postnatal hypergonadotropism manifest as a selective increase in LH. This hypergonadotropism may result from reduced sensitivity to estradiol (E 2 ) negative feedback and/or increased pituitary sensitivity to GnRH. We tested the hypothesis that excess T before birth reduces responsiveness of LH and FSH to E 2 negative feedback after birth. Pregnant ewes were treated with T propionate (100 mg/kg in cotton seed oil) or vehicle twice weekly from d 30 -90 gestation. Responsiveness to E 2 negative feedback was assessed at 12 and 24 wk of age in the ovaryintact female offspring. Our experimental strategy was first to arrest follicular growth and reduce endogenous E 2 by administering the GnRH antagonist (GnRH-A), Nal-Glu (50 g/kg sc every 12 h for 72 h), and then provide a fixed amount of exogenous E 2 via an implant. Blood samples were obtained every 20 min at 12 wk and every 10 min at 24 wk before treatment, during and after GnRH-A treatment both before and after E 2 implant. GnRH-A ablated LH pulsatility, reduced FSH by approximately 25%, and E 2 production diminished to near detection limit of assay at both ages in both groups. Prenatal T treatment produced a precocious and selective reduction in responsiveness of LH but not FSH to E 2 negative feedback, which was manifest mainly at the level of LH/GnRH pulse frequency. Collectively, these findings support the hypothesis that prenatal exposure to excess T decreases postnatal responsiveness to E 2 inhibitory feedback of LH/GnRH secretion to contribute to the development of hypergonadotropism. (Endocrinology 146: 4281-4291, 2005)

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Section: Discussionmentioning

confidence: 99%

“…Time points correspond to before GnRH-A administration (Pre), during GnRH-A administration, after cessation of GnRH-A administration (24,48, and 72 h), and during E 2 treatment. See Fig.…”

Section: Fig 5 Mean (N ϭ 7 Per Treatment Group) Concentrations Of Lmentioning

confidence: 99%

“…4). Blood samples were taken at 10-min intervals for 6 h before GnRH-A administration (Pre), thrice after cessation of GnRH-A treatment (24,48, and 72 h), and during E 2 implant. See Fig.…”

Section: Age-associated Changes In E 2 Negative Feedbackmentioning

confidence: 99%