Evidence that progesterone modulates anterior pituitary neuropeptide Y levels during the progesterone-induced gonadotropin surge in the estrogen-primed intact immature female rat

James L. O'Conner, Marlene F. Wade, Darrell W Brann, Virendra B. Mahesh

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18 Citations (Scopus)

Abstract

In a previous study we reported that in vivo estrogen-priming alone, without subsequent progester-one-treatment, was sufficient to maximize NPY potentiation of gonadotropin hormone-releasing hormone responsiveness exhibited in vitro by the rat anterior pituitary. This observation suggests that the necessity, as reported by others, for both estrogen-priming and progesterone-treatment to maximize NPY potentiation of GnRH responsiveness in vivo may be due to progesterone acting primarily at the hypothalamus. Consequently, the current study was performed to determine whether progesterone facilitates gonadotropin secretion in vivo by acting to stimulate hypothalamic synthesis of NPY and the subsequent elevation of anterior pituitary tissue levels of NPY. Intact immature female rats were injected with estradiol at 1700 h on days 27 and 28. On day 29 at 0900 h, the animals received an injection of progesterone (2 mg/kg) or vehicle and were subsequently sacrificed at 1200, 1330 and 1500 h. Rats which received only estradiol injections were used as controls. Surge levels of serum LH and FSH were observed at 1330 and 1500 h. Hypothalamic levels of NPY mRNA at 1200 h on day 29 were higher (P < 0.01) in estradiol-primed rats which received progester-one; there was no accompanying statistically significant change in hypothalamic NPY content. NPY content in the anterior pituitary was significantly increased (P < 0.01) at 1200 h on day 29 in estradiol-primed rats which received progesterone; there was no accompanying significant change in anterior pituitary NPY mRNA levels. Hypothalamic GnRH mRNA content was significantly increased (P < 0.01) at 1330 h on day 29 concomitant with the peak of the gonadotropin surge in the estradiol-primed, progesterone-treated rat. The data indicate that progesterone modulates hypothalamic NPY mRNA and anterior pituitary NPY levels as well as GnRH mRNA levels and that modulation of NPY levels in the hypothalamic-pituitary axis occurs prior to modulation of GnRH gene expression. These studies support the hypothesis that in the estrogen-primed rat, progesterone facilitates the induction of the gonadotropin surge by maintaining hypothalamic synthesis of NPY as well as by modulating anterior pituitary NPY tissue levels.

Original languageEnglish (US)
Pages (from-to)497-504
Number of pages8
JournalJournal of Steroid Biochemistry and Molecular Biology
Volume52
Issue number5
DOIs
StatePublished - Jan 1 1995

Fingerprint

Neuropeptide Y
Gonadotropins
Progesterone
Rats
Estrogens
Gonadotropin-Releasing Hormone
Estradiol
Messenger RNA
Modulation
Tissue
Injections
Gene expression
Hypothalamus
Animals
Hormones
Gene Expression
Therapeutics
Serum

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Clinical Biochemistry
  • Endocrinology
  • Molecular Biology
  • Molecular Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

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title = "Evidence that progesterone modulates anterior pituitary neuropeptide Y levels during the progesterone-induced gonadotropin surge in the estrogen-primed intact immature female rat",
abstract = "In a previous study we reported that in vivo estrogen-priming alone, without subsequent progester-one-treatment, was sufficient to maximize NPY potentiation of gonadotropin hormone-releasing hormone responsiveness exhibited in vitro by the rat anterior pituitary. This observation suggests that the necessity, as reported by others, for both estrogen-priming and progesterone-treatment to maximize NPY potentiation of GnRH responsiveness in vivo may be due to progesterone acting primarily at the hypothalamus. Consequently, the current study was performed to determine whether progesterone facilitates gonadotropin secretion in vivo by acting to stimulate hypothalamic synthesis of NPY and the subsequent elevation of anterior pituitary tissue levels of NPY. Intact immature female rats were injected with estradiol at 1700 h on days 27 and 28. On day 29 at 0900 h, the animals received an injection of progesterone (2 mg/kg) or vehicle and were subsequently sacrificed at 1200, 1330 and 1500 h. Rats which received only estradiol injections were used as controls. Surge levels of serum LH and FSH were observed at 1330 and 1500 h. Hypothalamic levels of NPY mRNA at 1200 h on day 29 were higher (P < 0.01) in estradiol-primed rats which received progester-one; there was no accompanying statistically significant change in hypothalamic NPY content. NPY content in the anterior pituitary was significantly increased (P < 0.01) at 1200 h on day 29 in estradiol-primed rats which received progesterone; there was no accompanying significant change in anterior pituitary NPY mRNA levels. Hypothalamic GnRH mRNA content was significantly increased (P < 0.01) at 1330 h on day 29 concomitant with the peak of the gonadotropin surge in the estradiol-primed, progesterone-treated rat. The data indicate that progesterone modulates hypothalamic NPY mRNA and anterior pituitary NPY levels as well as GnRH mRNA levels and that modulation of NPY levels in the hypothalamic-pituitary axis occurs prior to modulation of GnRH gene expression. These studies support the hypothesis that in the estrogen-primed rat, progesterone facilitates the induction of the gonadotropin surge by maintaining hypothalamic synthesis of NPY as well as by modulating anterior pituitary NPY tissue levels.",
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T1 - Evidence that progesterone modulates anterior pituitary neuropeptide Y levels during the progesterone-induced gonadotropin surge in the estrogen-primed intact immature female rat

AU - O'Conner, James L.

AU - Wade, Marlene F.

AU - Brann, Darrell W

AU - Mahesh, Virendra B.

PY - 1995/1/1

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N2 - In a previous study we reported that in vivo estrogen-priming alone, without subsequent progester-one-treatment, was sufficient to maximize NPY potentiation of gonadotropin hormone-releasing hormone responsiveness exhibited in vitro by the rat anterior pituitary. This observation suggests that the necessity, as reported by others, for both estrogen-priming and progesterone-treatment to maximize NPY potentiation of GnRH responsiveness in vivo may be due to progesterone acting primarily at the hypothalamus. Consequently, the current study was performed to determine whether progesterone facilitates gonadotropin secretion in vivo by acting to stimulate hypothalamic synthesis of NPY and the subsequent elevation of anterior pituitary tissue levels of NPY. Intact immature female rats were injected with estradiol at 1700 h on days 27 and 28. On day 29 at 0900 h, the animals received an injection of progesterone (2 mg/kg) or vehicle and were subsequently sacrificed at 1200, 1330 and 1500 h. Rats which received only estradiol injections were used as controls. Surge levels of serum LH and FSH were observed at 1330 and 1500 h. Hypothalamic levels of NPY mRNA at 1200 h on day 29 were higher (P < 0.01) in estradiol-primed rats which received progester-one; there was no accompanying statistically significant change in hypothalamic NPY content. NPY content in the anterior pituitary was significantly increased (P < 0.01) at 1200 h on day 29 in estradiol-primed rats which received progesterone; there was no accompanying significant change in anterior pituitary NPY mRNA levels. Hypothalamic GnRH mRNA content was significantly increased (P < 0.01) at 1330 h on day 29 concomitant with the peak of the gonadotropin surge in the estradiol-primed, progesterone-treated rat. The data indicate that progesterone modulates hypothalamic NPY mRNA and anterior pituitary NPY levels as well as GnRH mRNA levels and that modulation of NPY levels in the hypothalamic-pituitary axis occurs prior to modulation of GnRH gene expression. These studies support the hypothesis that in the estrogen-primed rat, progesterone facilitates the induction of the gonadotropin surge by maintaining hypothalamic synthesis of NPY as well as by modulating anterior pituitary NPY tissue levels.

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