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Rodent Models of Non-classical Progesterone Action Regulating Ovulation.

Melinda A Mittelman-Smith1, Lauren M Rudolph1, Margaret A Mohr1

  • 1Department of Neurobiology, David Geffen School of Medicine at UCLA, The Laboratory of Neuroendocrinology, Brain Research Institute, University of California Los Angeles, Los Angeles, CA, United States.

Frontiers in Endocrinology
|August 10, 2017
PubMed
Summary
This summary is machine-generated.

Steroid hormones, like estrogen and progesterone, signal rapidly through cell membranes, not just the nucleus. This non-classical pathway influences cellular functions and reproductive behaviors.

Keywords:
estrogenhypothalamuskisspeptinlordosisluteinizing hormoneovulationprogesteronereproduction

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Area of Science:

  • Endocrinology
  • Neurobiology
  • Cellular Signaling

Background:

  • Steroid hormones traditionally bind nuclear receptors for transcriptional regulation.
  • Emerging evidence shows rapid, non-genomic actions mediated by cell membrane receptors.
  • Estrogen receptor alpha (ERα) exemplifies membrane-initiated steroid hormone signaling.

Purpose of the Study:

  • To review the non-classical signaling of progesterone (P4).
  • To compare P4 membrane signaling with estrogen (E2) neurotransmitter-like actions.
  • To discuss the role of these pathways in rodent reproductive behaviors.

Main Methods:

  • Literature review of studies on steroid hormone membrane signaling.
  • Comparative analysis of estrogen and progesterone non-genomic pathways.
  • Focus on findings related to reproductive behaviors in rodents.

Main Results:

  • Progesterone initiates rapid intracellular signaling cascades via membrane receptors.
  • These non-genomic effects include calcium release and kinase activation.
  • Parallels exist between E2 and P4 membrane-initiated signaling.

Conclusions:

  • Progesterone exhibits rapid, non-transcriptional signaling at the cell membrane.
  • Membrane-initiated steroid hormone actions are crucial for reproductive behaviors.
  • Further research into non-classical steroid hormone signaling is warranted.