Progesterone enhances the surge of luteinizing hormone by increasing the activation of luteinizing hormone-releasing hormone neurons

Wen Sen Lee, M. Susan Smith, Gloria E. Hoffman

Research output: Contribution to journalArticle

114 Citations (Scopus)

Abstract

The ability of progesterone (P) to enhance the surge of LH in the rat is well documented, but whether its primary site of action is on the pituitary or brain is unclear. To determine whether P can alter the activation of LHRH neurons, 1) intact female rats were treated with the P antagonist RU486 (5 mg) at 1230 h on proestrus and killed at specified times during the afternoon and evening for comparison of plasma LH levels and cFos expression in LHRH neurons with untreated proestrous rats. RU486 treatment greatly reduced both the magnitude of the LH surge and the degree of cFos induction (numbers of cells expressing cFos and intensity of cFos staining) in LHRH neurons during proestrus. 2) Ovariectomized (OVX) rats were primed with estradiol benzoate (EB, 1 μg) and then were treated with EB alone (50 μg) or EB plus P (5 mg). Treatment with EB without P resulted in significantly lower peak LH levels and a reduced cFos response in LHRH neurons than the EB-P treated rats. These data suggest that the actions of P eventuate in an enhanced activation of LHRH neurons that may be responsible for the increased magnitude of the LH surge.

Original languageEnglish
Pages (from-to)2604-2606
Number of pages3
JournalEndocrinology
Volume127
Issue number5
Publication statusPublished - Nov 1990
Externally publishedYes

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Luteinizing Hormone
Gonadotropin-Releasing Hormone
Progesterone
Neurons
Proestrus
Cell Count
Staining and Labeling
Brain

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Progesterone enhances the surge of luteinizing hormone by increasing the activation of luteinizing hormone-releasing hormone neurons. / Lee, Wen Sen; Smith, M. Susan; Hoffman, Gloria E.

In: Endocrinology, Vol. 127, No. 5, 11.1990, p. 2604-2606.

Research output: Contribution to journalArticle

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