Display Settings:


Send to:

Choose Destination
See comment in PubMed Commons below
Front Neurosci. 2013 Sep 19;7:159. doi: 10.3389/fnins.2013.00159.

Non-genomic mechanisms of progesterone action in the brain.

Author information

  • 1Department of Pharmacology and Neuroscience, Center FOR HER, Institute for Aging and Alzheimer's Disease Research, University of North Texas Health Science Center at Fort Worth Fort Worth, TX, USA.


Progesterone is a gonadal steroid hormone whose physiological effects extend well beyond the strict confines of reproductive function. In fact, progesterone can have important effects on a variety of tissues, including the bone, the heart and the brain. Mechanistically, progesterone has been thought to exert its effects through the progesterone receptor (PR), a member of the nuclear steroid hormone superfamily, and as such, acts through specific progesterone response elements (PRE) within the promoter region of target genes to regulate transcription of such genes. This has been often described as the "genomic" mechanism of progesterone action. However, just as progesterone has a diverse range of tissue targets, the mechanisms through which progesterone elicits its effects are equally diverse. For example, progesterone can activate alternative receptors, such as membrane-associated PRs (distinct from the classical PR), to elicit the activation of several signaling pathways that in turn, can influence cell function. Here, we review various non-nuclear (i.e., non-genomic) signaling mechanisms that progesterone can recruit to elicit its effects, focusing our discussion primarily on those signaling mechanisms by which progesterone influences cell viability in the brain.


brain; non-genomic; progesterone; progesterone receptor; signaling

Free PMC Article

Images from this publication.See all images (1)Free text

Figure 1
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Icon for Frontiers Media SA Icon for PubMed Central
    Loading ...
    Write to the Help Desk