Role of proestrous progesterone secretion in suppressing basal pulsatile LH secretion during estrus of the estrous cycle

M (Susan) Smith, Susan R. Fox, Robert T. Chatterton

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

These studies examined the mechanisms responsible for the paucity of basal LH pulses during estrus. We confirmed our earlier observations that constant infusion of naloxone during estrus results in the immediate appearance of pulsatile LH secretion during estrus, consisting of LH peak heights and LH interpulse intervals that are similar to those observed during other days of the estrous cycle. We then tested whether the proestrous surge of progesterone was responsible for the suppression of pulsatile LH secretion during estrus. Three treatment regimens were used on proestrus to either block progesterone secretion (pentobarbital) or block its action (progesterone antiserum or the progesterone antagonist. RU 486). After treatment at 12.00 h on proestrus, blood samples were collected during estrus every 10 min for 4 h, and the plasma samples were analyzed for the pattern of LH secretion. Treatment with pentobarbital (35 mg/kg at 12:00 h) blocked the proestrous surges of LH and progesterone and resulted in pulsatile LH secretion during estrus. The LH interpulse interval (72 ± 7 min) was somewhat slower than that observed in the naloxone-infused animals (54 ± 8 min). Simultaneous treatment with pentobarbital and progesterone at 12:00 h on proestrus completely prevented the appearance of LH pulses during estrus. Treatment with either progesterone antiserum (0.5 ml, i.v.) or RU 486 (1 mg s.c.) resulted in the initiation of pulsatile LH secretion during estrus. In the RU 486-treated animals, LH peak heights and LH interpulse intervals were similar to those observed in naloxone-infused animals and during other days of the estrous cycle. These studies demonstrate that the suppression of pulsatile LH secretion during estrus is dependent on endogenous opioid tone. In addition, the proestrous surge of progesterone may be responsible for this suppression during estrus, since blocking progesterone secretion or blocking its action restores pulsatile LH secretion on estrus. We hypothesize that the proestrous surge of progesterone may cause an increase in endogenous opioid tone which then suppresses GnRH release and pulsatile LH secretion during estrus.

Original languageEnglish (US)
Pages (from-to)308-314
Number of pages7
JournalNeuroendocrinology
Volume50
Issue number3
DOIs
StatePublished - 1989
Externally publishedYes

Fingerprint

Estrous Cycle
Estrus
Progesterone
Proestrus
Mifepristone
Pentobarbital
Naloxone
Opioid Analgesics
Immune Sera
Gonadotropin-Releasing Hormone

Keywords

  • Endogenous opioid tone
  • Estrus
  • GnRH
  • Proestrous
  • Progesterone
  • Pulsatile LH
  • Suppression

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Cellular and Molecular Neuroscience
  • Endocrine and Autonomic Systems
  • Neuroscience(all)

Cite this

Role of proestrous progesterone secretion in suppressing basal pulsatile LH secretion during estrus of the estrous cycle. / Smith, M (Susan); Fox, Susan R.; Chatterton, Robert T.

In: Neuroendocrinology, Vol. 50, No. 3, 1989, p. 308-314.

Research output: Contribution to journalArticle

Smith, M (Susan) ; Fox, Susan R. ; Chatterton, Robert T. / Role of proestrous progesterone secretion in suppressing basal pulsatile LH secretion during estrus of the estrous cycle. In: Neuroendocrinology. 1989 ; Vol. 50, No. 3. pp. 308-314.
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AB - These studies examined the mechanisms responsible for the paucity of basal LH pulses during estrus. We confirmed our earlier observations that constant infusion of naloxone during estrus results in the immediate appearance of pulsatile LH secretion during estrus, consisting of LH peak heights and LH interpulse intervals that are similar to those observed during other days of the estrous cycle. We then tested whether the proestrous surge of progesterone was responsible for the suppression of pulsatile LH secretion during estrus. Three treatment regimens were used on proestrus to either block progesterone secretion (pentobarbital) or block its action (progesterone antiserum or the progesterone antagonist. RU 486). After treatment at 12.00 h on proestrus, blood samples were collected during estrus every 10 min for 4 h, and the plasma samples were analyzed for the pattern of LH secretion. Treatment with pentobarbital (35 mg/kg at 12:00 h) blocked the proestrous surges of LH and progesterone and resulted in pulsatile LH secretion during estrus. The LH interpulse interval (72 ± 7 min) was somewhat slower than that observed in the naloxone-infused animals (54 ± 8 min). Simultaneous treatment with pentobarbital and progesterone at 12:00 h on proestrus completely prevented the appearance of LH pulses during estrus. Treatment with either progesterone antiserum (0.5 ml, i.v.) or RU 486 (1 mg s.c.) resulted in the initiation of pulsatile LH secretion during estrus. In the RU 486-treated animals, LH peak heights and LH interpulse intervals were similar to those observed in naloxone-infused animals and during other days of the estrous cycle. These studies demonstrate that the suppression of pulsatile LH secretion during estrus is dependent on endogenous opioid tone. In addition, the proestrous surge of progesterone may be responsible for this suppression during estrus, since blocking progesterone secretion or blocking its action restores pulsatile LH secretion on estrus. We hypothesize that the proestrous surge of progesterone may cause an increase in endogenous opioid tone which then suppresses GnRH release and pulsatile LH secretion during estrus.

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