Progesterone, but Not LHRH or Prostaglandin E₂, Induces Sequential Inhibition of Lordosis to Various Lordogenic Agents

Abstract

In experiment I we studied the capacity of progesterone (P) and two nonsteroidal agents that activate lordosis, but do not bind to the progestin receptor (PR), i.e. luteinizing hormone-releasing hormone (LHRH) and prostaglandin E₂ (PGE₂) to induce sequential inhibition (SI) in ovariectomized estradiol-primed rats. The administration of 1 mg P, 5 µg LHRH or 100 µg PGE₂ induced significant lordosis within 4 h. An injection of 1 mg P, 24 h after the administration of the above lordogenic agents, induced significant lordosis in rats pretreated with LHRH or PGE₂, but not in those pretreated with P. Thus, only P induced SI (p < 0.025). In experiment II we investigated if progestin-induced SI results in a reduced capacity of the subjects to respond only to P or to other lordogenic agents. The synthetic progestin norgestrel (400 µg administered 24 h earlier) significantly reduced the responsiveness to P (p < 0.01), LHRH (p < 0.01), PGE₂ (p < 0.025) and dibutyryl cyclic AMP (db cAMP p < 0.01). Results suggest that SI is triggered only by agents that bind to the PR (experiment I) and that it decreases the responsiveness of rats not only to P but also to other lordogenic agents (experiment II).

Nitric oxide and ERK/MAPK mediation of estrous behavior induced by GnRH, PGE2 and db-cAMP in rats

“…These results agree with previous experiments administering these chemicals both through intracerebral and sc routes [4, 7–9, 11, 33, 38, 60–64]. The data also show that the icv infusion of a NOS inhibitor, L-NAME, and an inhibitor of NO-stimulated guanylyl cyclase, ODQ, significantly attenuates the lordosis behavior induced by GnRH, PGE 2 and db-cAMP, especially at the 1 and 2 hr tests.…”

Progesterone Inhibits Female Courtship Behavior in Domestic Canaries (Serinus canaria)

“…It is noteworthy that progesterone was found to exert a suppressive effect on female sexual behavior in reptiles (Godwin et al, 1996) as well as in birds (El Halawani et al, 1986; and present study) and mammals (Blaustein and Wade, 1977;González-Mariscal et al, 1993). The consistency of progesterone effects among species of different vertebrate classes supports the hypothesis of Godwin and co-workers (1996) that the decrease in sexual behavior following plasma progesterone increase might represent an "evolutionarily conserved mechanism in the regulation of female sexual behavior.…”

“…Gonadal steroids exert modulating influences upon the central nervous system, resulting in physiological as well as behavioral changes (Mani, Blaustein, and O' Malley, 1997). In rodents, progesterone initially facilitates and later inhibits sexual receptivity (Blaustein and Wade, 1977;González-Mariscal, Melo, and Beyer, 1993).…”

“…A suppressive effect of progesterone on female sexual behavior was incidentally observed in a study dealing with the control of nesting in ovariectomized turkey hens (Meleagris gallopavo) (El Halawani, Silsby, Behnke, and Fehrer, 1986); in this study, estradiol-primed hens showed sexual squatting whereas females treated with estradiol and progesterone failed to show sexual activity. Suppressive effects of progesterone on female sexual behavior have been clearly established in lizards (Godwin, Hartman, Grammer, and Crews, 1996) as well as in rodents (Blaustein and Wade, 1977;González-Mariscal et al, 1993).…”

Src kinase signaling mediates estrous behavior induced by 5β-reduced progestins, GnRH, prostaglandin E2 and vaginocervical stimulation in estrogen-primed rats

“…4, the PR-Src-MAPK pathway can also modulate the nuclear PR by phosphorylating serine 294, a process that enhances the transcriptional activity of the PR and targets it for subsequent degradation by the 26S proteasome (Camacho-Arroyo et al, 2002;Faivre et al, 2005;Lange et al, 1998;Qiu and Lange, 2003). Although this could constitute a process through which GnRH, PGE 2 or the 5β progestins stimulate lordosis behavior, the fact that these agents do not cause sequential inhibition of lordosis (González-Flores et al, 2004a;González-Mariscal et al, 1993), a process resulting from ser294 phosphorylation of the PR (Lange et al, 2000;Shen et al, 2001), does not support this idea.…”