Effects of progesterone or neuroactive steroid?

A. Leslie Morrow (), Margaret J. VanDoren () and Leslie L. Devaud ()
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A. Leslie Morrow: and Center for Alcohol Studies, University of North Carolina School of Medicine
Margaret J. VanDoren: University of North Carolina School of Medicine
Leslie L. Devaud: University of North Carolina School of Medicine

Nature, 1998, vol. 395, issue 6703, 652-652

Abstract: Abstract Smith et al.1 reported some interesting results about the effects of progesterone treatment and withdrawal on the gene encoding the GABAAreceptor α4 subunit, a constituent of receptors for the neurotransmitter GABA (γ-aminobutyric acid). However, we disagree with their conclusion that the effects of progesterone withdrawal are mediated by reduced levels in the brain of the GABAAreceptor active neurosteroid 3α-OH-5α-pregnan-20-one (3α,5α-THP, or allopregnanalone). The ability of indomethacin to reverse the effects of progesterone was interpreted as evidence that the effects of progesterone were mediated by 3α,5α-THP. Smith et al.1 did not provide direct evidence that levels of 3α,5α-THP were reduced by indomethacin (which reversed the effects of progesterone), or that progesterone levels were not altered by indomethacin. In some cases, indomethacin can increase progesterone levels directly2, which may explain why indomethacin can reverse the effects of progesterone withdrawal.

Date: 1998
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DOI: 10.1038/27106

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