Skip to main content
. 2013 Aug 7;7:138. doi: 10.3389/fnins.2013.00138

Table 1.

Studies of progesterone inhibition of OXTR signaling.

Species Citation Major findings
Rodent Putnam et al., 1991 P and P metabolites rapidly inhibit contractions of rat uteri within 2 min of treatment
Effect of P not opposed by treatment with the PGR antagonist RU 486
Grazzini et al., 1998 P reduced rat uterine OT signaling without a change in Oxtr mRNA expression
Inhibition due to a P-mediated decrease in OT binding capacity, not binding affinity
Occurred at the level of the plasma membrane
Specific and high affinity binding sites for P only in transfected CHO cells expressing Oxtr with high affinity
Regulated by the state of the G-protein coupling to the receptor
Ovine Dunlap and Stormshak, 2004 Isolated membrane fractions pre-incubated with P showed decreased OT binding, reversed by co-incubation with RU 486
High affinity binding site for P
P, R5020 (synthetic progestin), RU 486, and OT all bind to the same site pre-exposure of membranes to P significantly increased the number of P binding sites
Bishop and Stormshak, 2006 P binding to endometrial membranes is dose dependent
Inhibition of both OT-induced IP3 accumulation and PGF release from ovine endometrial explants by P within hours of exposure
Bishop et al., 2008 Rapid, specific inhibition of OXTR signaling by P in COS7 cells transfected with the ovine OXTR that lack PGRs
P did not decrease specific binding of OT
No specific P binding sites in membranes of OXTR-transfected cells
Bovine Bogacki et al., 2002 P inhibited OT binding at all concentrations (20–0.002 μM) investigated
OT-induced intracellular calcium release and PGF secretion by bovine endometrial tissue explants in the presence of actinomycin D
Duras et al., 2005 P as well as pregnenolone, 17β-hydroxyprogesterone, the PR antagonist onapristone, and testosterone at μM concentrations were all able to interfere with OT-stimulated PGF secretion and intracellular calcium release
Davis et al., 2010 P at μM concentration rapidly (within 1 h) inhibited OT-induced Ca2+ release from endoplasmic reticulum of small steroidogenic luteal cells, possibly via exclusion of cholesterol from the luteal cell plasma membrane
Primate/Human Burger et al., 1999 μM concentration of P inhibited the signaling of several related GPCRs as well as the OXTR
Chanrachakul et al., 2005 Within 20 min-1 h P decreased OT-induced contractility of term myometrium in a concentration dependent manner
Maximal inhibition at 10 μM P