Progesterone-Like Effects of Estradiol on Reproductive Behavior and Hypothalamic Progestin Receptors in the Female Rat

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Abstract
During the rat estrous cycle, estradiol (E2) and progesterone (P) synergize to activate reproductive behavior. However, receptivity and proceptivity can be elicited by E2 alone in ovariectomized (OVX) animals, particularly when E2 doses are high. The purpose of this study was to determine the neuroendocrine mechanism by which E2 elicits P-dependent reproductive behavior. Adult OVX females received estrogen treatment for 72 h, which consisted of 5 mm Silastic capsules containing 100% E2 or 10% E2, or of 3 injections of estradiol benzoate (EB; 20 µg daily). At 72 h, some animals were sacrificed for nuclear progestin receptor (NPR) measurements, while others were tested for reproductive behavior. The remaining animals received 1 -mg injections of E2, P, moxestrol (Mox) or oil, and either were sacrificed 2 h later for NPR measurements or were tested 4 h later for reproductive behavior. A subset of the animals receiving 1 mg E2 received concurrent administration of the protein synthesis inhibitor, anisomycin (ANI; 100 mg/kg). Acute administration of 1 mg of E2 or P significantly elevated proceptivity, receptivity and NPRs in the mediobasal hypothalamus-preoptic area (MBH-POA) and pituitary (PIT) in females primed with 100% E2. An equivalent dose of Mox was without effect. ANI blocked the acute activation of feminine reproductive behavior by 1 mg of E2. In the absence of acute steroid administration, animals primed for 72 h with EB showed higher levels of reproductive behavior than animals primed with 100% E2. Likewise, as the dose of estrogen administered in the priming regimen was increased, the level of NPR in the MBH-POA and PIT increased in the absence of acute steroid (EB > 100% E2 > 10% E2). These results suggest that the actions of E2 via estrogen receptors are not by themselves sufficient to activate feminine reproductive behavior in the rat. The display of high levels of proceptivity and receptivity requires the subsequent activation of neural progestin receptors by P or by E2.

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