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Facilitation or inhibition of the oestradiol-induced gonadotrophin surge in the immature female rat by progesterone: effects on pituitary responsiveness to gonadotrophin-releasing hormone (GnRH), GnRH self-priming and pituitary mRNAs for the progesterone receptor A and B isoforms.
J Neuroendocrinol. 2007 Dec; 19(12):988-1000.JN

Abstract

Progesterone can either facilitate or inhibit the oestradiol (E(2))-induced gonadotrophin surge. We have previously developed immature female rat models to characterise and investigate the mechanisms of progesterone inhibition or facilitation. The aim of the present study was to determine the role of pituitary responsiveness to gonadotrophin-releasing hormone (GnRH) and GnRH self-priming under conditions of progesterone-facilitation and progesterone-inhibition, and whether the underlying mechanisms reflect changes in mRNAs encoding the A and B isoforms of the progesterone receptor (PR) in the pituitary gland. Pituitary responsiveness to GnRH, determined by measuring the luteinising hormone (LH) response to one i.v. injection of GnRH, was decreased by 60-80% (P < 0.001) in the progesterone-inhibition model. GnRH self-priming, estimated as the increment in the LH response to the second of two injections of GnRH separated by 60 min, was also significantly reduced (P < 0.05) in this model. In the progesterone-facilitation model, the LH response to GnRH injection was increased 2.5-3-fold (P < 0.05), an effect suppressed by the progesterone receptor antagonist, mifepristone. Progesterone-facilitation of LH release and increased pituitary responsiveness to GnRH were blocked by sheep anti-GnRH serum injected i.v. immediately after insertion of progesterone implants. The PR-B mRNA isoform, measured by solution hybridisation/RNase protection assay, was the predominant form in the pituitary of the immature female rat. PR-B was increased by E(2) and decreased by progesterone in both models. Thus, in immature female rats, progesterone-inhibition of the E(2)-induced LH surge is due to significant reduction in pituitary responsiveness to GnRH as well as in the magnitude of GnRH self-priming. Progesterone-facilitation of the E(2)-induced LH surge is due to increased pituitary responsiveness to GnRH, which is mediated by PR, and depends on endogenous GnRH release. The differences between progesterone-facilitation and progesterone-inhibition are not due to differences in regulation of pituitary PR-B mRNA.

Authors+Show Affiliations

Department of Neurobiology and Behavior, The Rockefeller University, New York, NY, USA. bjattardi@bioqual.comNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

18001329

Citation

Attardi, B, et al. "Facilitation or Inhibition of the Oestradiol-induced Gonadotrophin Surge in the Immature Female Rat By Progesterone: Effects On Pituitary Responsiveness to Gonadotrophin-releasing Hormone (GnRH), GnRH Self-priming and Pituitary mRNAs for the Progesterone Receptor a and B Isoforms." Journal of Neuroendocrinology, vol. 19, no. 12, 2007, pp. 988-1000.
Attardi B, Scott R, Pfaff D, et al. Facilitation or inhibition of the oestradiol-induced gonadotrophin surge in the immature female rat by progesterone: effects on pituitary responsiveness to gonadotrophin-releasing hormone (GnRH), GnRH self-priming and pituitary mRNAs for the progesterone receptor A and B isoforms. J Neuroendocrinol. 2007;19(12):988-1000.
Attardi, B., Scott, R., Pfaff, D., & Fink, G. (2007). Facilitation or inhibition of the oestradiol-induced gonadotrophin surge in the immature female rat by progesterone: effects on pituitary responsiveness to gonadotrophin-releasing hormone (GnRH), GnRH self-priming and pituitary mRNAs for the progesterone receptor A and B isoforms. Journal of Neuroendocrinology, 19(12), 988-1000.
Attardi B, et al. Facilitation or Inhibition of the Oestradiol-induced Gonadotrophin Surge in the Immature Female Rat By Progesterone: Effects On Pituitary Responsiveness to Gonadotrophin-releasing Hormone (GnRH), GnRH Self-priming and Pituitary mRNAs for the Progesterone Receptor a and B Isoforms. J Neuroendocrinol. 2007;19(12):988-1000. PubMed PMID: 18001329.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Facilitation or inhibition of the oestradiol-induced gonadotrophin surge in the immature female rat by progesterone: effects on pituitary responsiveness to gonadotrophin-releasing hormone (GnRH), GnRH self-priming and pituitary mRNAs for the progesterone receptor A and B isoforms. AU - Attardi,B, AU - Scott,R, AU - Pfaff,D, AU - Fink,G, PY - 2007/11/16/pubmed PY - 2008/1/3/medline PY - 2007/11/16/entrez SP - 988 EP - 1000 JF - Journal of neuroendocrinology JO - J Neuroendocrinol VL - 19 IS - 12 N2 - Progesterone can either facilitate or inhibit the oestradiol (E(2))-induced gonadotrophin surge. We have previously developed immature female rat models to characterise and investigate the mechanisms of progesterone inhibition or facilitation. The aim of the present study was to determine the role of pituitary responsiveness to gonadotrophin-releasing hormone (GnRH) and GnRH self-priming under conditions of progesterone-facilitation and progesterone-inhibition, and whether the underlying mechanisms reflect changes in mRNAs encoding the A and B isoforms of the progesterone receptor (PR) in the pituitary gland. Pituitary responsiveness to GnRH, determined by measuring the luteinising hormone (LH) response to one i.v. injection of GnRH, was decreased by 60-80% (P < 0.001) in the progesterone-inhibition model. GnRH self-priming, estimated as the increment in the LH response to the second of two injections of GnRH separated by 60 min, was also significantly reduced (P < 0.05) in this model. In the progesterone-facilitation model, the LH response to GnRH injection was increased 2.5-3-fold (P < 0.05), an effect suppressed by the progesterone receptor antagonist, mifepristone. Progesterone-facilitation of LH release and increased pituitary responsiveness to GnRH were blocked by sheep anti-GnRH serum injected i.v. immediately after insertion of progesterone implants. The PR-B mRNA isoform, measured by solution hybridisation/RNase protection assay, was the predominant form in the pituitary of the immature female rat. PR-B was increased by E(2) and decreased by progesterone in both models. Thus, in immature female rats, progesterone-inhibition of the E(2)-induced LH surge is due to significant reduction in pituitary responsiveness to GnRH as well as in the magnitude of GnRH self-priming. Progesterone-facilitation of the E(2)-induced LH surge is due to increased pituitary responsiveness to GnRH, which is mediated by PR, and depends on endogenous GnRH release. The differences between progesterone-facilitation and progesterone-inhibition are not due to differences in regulation of pituitary PR-B mRNA. SN - 0953-8194 UR - https://www.unboundmedicine.com/medline/citation/18001329/Facilitation_or_inhibition_of_the_oestradiol_induced_gonadotrophin_surge_in_the_immature_female_rat_by_progesterone:_effects_on_pituitary_responsiveness_to_gonadotrophin_releasing_hormone__GnRH__GnRH_self_priming_and_pituitary_mRNAs_for_the_progesterone_receptor_A_and_B_isoforms_ L2 - https://doi.org/10.1111/j.1365-2826.2007.01613.x DB - PRIME DP - Unbound Medicine ER -