Progesterone prevents corticosterone mediated inhibition of estrous behaviour in rats.

Stress induced by application of electric foot shocks (300 microA/shock, five shocks per episode, 4 episodes at 1800, 1830, 1900 and 1930 hrs on the proestrus day) to rats at the time of pre-ovulatory progesterone secretion, abolished lordosis and resulted in maximum rejection co-efficient, whereas treatment with a CRF receptor antagonist (alpha-helical CRF9-41) or metapirone, an inhibitor of corticosterone synthesis, prior to application of the electric foot shocks, resulted in normal lordosis and a significant reduction in rejection coefficient. Further, administration of a single dose of corticosterone (40 microg) at 1800 hrs of proestrus caused inhibition of lordosis and resulted in maximum rejection co-efficient. On the other hand, corticosterone + progesterone treatment at 1800 hrs of proestrus resulted in normal lordosis and a significant reduction in rejection coefficient. The facts that stress induced inhibition of lordosis is prevented by CRF receptor antagonist or metapirone and that corticosterone inhibits lordosis indicate that stress induced inhibition of lordosis is mediated by corticosterone. Further, normal display of lordosis by rats treated with corticosterone + progesterone in contrast to its absence in corticosterone alone treated rats suggests that impaired progesterone secretion due to action of corticosterone leads to inhibition of lordosis.