Control of proceptive and receptive behavior by ovarian hormones in the Syrian hamster (Mesocricetus auratus)

Two studies examined the roles of estrogen with progesterone and of estrogen alone on the proceptive and receptive behavior of female hamsters. Proceptivity was measured in terms of proximity (approaching, leaving, and following by the female) and in time spent sniffing the male partner. During the 4-day natural estrous cycle, these measures change systematically although lordosis is seen only on Day 1 (estrus). With a constant dose of progesterone, both proceptive and receptive behavior were found to be estrogen dose dependent in ovariectomized females. At estrogen levels too low to induce lordosis, changes in proceptive behavior were seen; at the two highest levels of estrogen, lordosis was maximal but proceptive behavior continued to increase. With estrogen alone, levels of proceptive behavior were attained characteristic both of estrus and of the higher estrogen and progesterone dosage but were not accompanied by spontaneous lordosis. Factors indicating that proceptivity and receptivity may be under separate hormonal and neural control are discussed.     

Comparison of some CNS effects of luteinizing hormone-releasing hormone and progesterone

Luteinizing hormone-releasing hormone (LHRH) has been reported to facilitate lordotic behavior in estrogen-primed ovariectomized (OVX) female rats in a manner similar to progesterone (P). This study compared P and LHRH with respect to their behavioral effects and site of action within the brain. The hormones were compared using two different components of sexual behavior, receptivity and proceptivity. To test for receptivity, OVX females were given behaviorally ineffective estradiol benzoate (EB) injections sc 48 hr before testing. They were then treated with either P, LHRH, or vehicle by various routes. Two and/or four hours later, receptivity (LQ) was measured. Treatments for the proceptivity test were similar except that a larger EP-priming dose, which facilitates preceptive behavior, was used. Four hours later, LQ and hopping, darting, and earwiggling were scored. In the receptivity test, sc administration of 1 mg P or 1 μg LHRH (but not 0.5 or 5.0 μg) significantly elevated LQ with respect to vehicle injection 4 hr after treatment. In the proceptivity test, 0.5, 1.0, and 5.0 μg of LHRH given sc failed to alter significantly either LQ or soliciting behavior. Progesterone facilitated both parameters. Implantation of crystalline P into the midbrain reticular formation (MRF) has been shown to elicit both the receptive and preceptive effects of the steroid. Microinjection of as much as 100 ng of LHRH in 1.0 μl saline into the same region failed to enhance lordotic behavior compared to saline injection alone, while a 200-ng intracerebroventricular dose significantly facilitated lordosis at 4 hr. The data indicate that LHRH does not induce proceptive behavior. The effects of peripherally administered LHRH on receptive behavior are similar but less pronounced than those of P. The two hormones elicit this effect from different sites in the brain.     

Sexual differentiation of reproductive behavior in pigs: defeminizing effects of prepubertal estradiol

The present study sought to determine (1) whether estrogen by itself can defeminize the behavior of pigs during the late juvenile-early pubertal period, and (2) whether the progressive late defeminization reported for pigs is a true organizational effect, as opposed to an artifact of the time between castration and testing. Male pigs were castrated at 19-22 days or left intact and females were ovariectomized at 3 months. Additional males castrated at 19-22 days and females ovariectomized at 3 months were implanted with estradiol benzoate (EB) from 3 to 5.5 months. After castration of the previously intact males at the age of 5.5 months, all subjects were tested beginning at 6.5 months for proceptivity (choice of a male versus a female in a T-maze) and receptivity (immobilization to a mounting male) following an injection of EB. EB administered during development significantly defeminized proceptivity and receptivity in both sexes. The decrease in proceptivity was more pronounced in males than in females and was more pronounced than the decrease in receptivity, as if differentiation ends earlier for proceptivity than for receptivity; the decrease in receptivity was more pronounced in females. To see whether the capacity to display female-typical behavior is a function of time since castration, we castrated additional males at 4 months and tested for receptivity 9 days later following an injection of EB, then tested again with the other subjects at 6.5 months. The proceptivity and receptivity scores for males castrated at 4 months fell between those for intact males and males castrated at 3 weeks, and thus these animals were not completely defeminized. They were more receptive at 6.5 months than at 4 months, but the difference was not significant. These results indicate that in pigs estradiol defeminizes both receptive and proceptive behavior and that this defeminization can occur relatively late in development.     

Sexual characteristics of female dogs during successive phases of the ovarian cycle

Five female beagles were examined periodically throughout their second biannual cycle of proestrus, estrus, metestrus, and anestrus for fluctuations in several physiological and behavioral charateristics. Physiological measures included plasma levels of estradiol and progesterone as well as the vulvar swelling and vaginal bleeding that begin with proestrus and continue in estrus. Behavioral tests revealed changes in female receptivity, attractivity, and proceptivity. Estradiol increased prior to the onset of proestrus and declined during estrus. Progesterone levels were low during most of proestrus, increased from the beginning to the end of estrus, and remained elevated during the first month or more of metestrus. While they were in proestrous females were not receptive but they and their vaginal secretions were highly attractive to males. Attractivity remained high throughout estrus and declined abruptly in the next 24 hr. Receptivity increased over the first 3 days of estrus and continued at a high level until the last 3 days during which it decreased slightly, and then dropped nearly to zero within the next 24 hr. “Sexual reflexes” of the vulva, tail, and hindquarters followed the same course of changes described for attractivity. Proceptive behavior, including seeking proximity to caged males and display of solicitation responses during mating tests was characteristic of females during proestrus and estrus but uncommon or absent in other phases of the cycle. It is hypothesized that in the natural cycle, attractivity and proceptivity develop during proestrus as a consequence of rapidly increasing secretion of estrogen. The onset of receptivity is due to synergistic action of estrogen and progesterone. Estrogen secreted during proestrus primes the system, and progesterone secreted just before and during estrus activates it. Termination of receptivity is thought to be due to the marked decline in estrogen, to inhibition by high concentrations of progesterone, or to a combination of these factors.     

Sex differences in response to discrete estradiol injections

Developmental effects of perinatal androgens render adult male rats refractory to the activation of feminine sexual behavior by estradiol (E2) and progesterone (P). Recent evidence suggested that fluctuating levels of systemic E2, which are thought to approximate the ovarian secretion under physiological conditions, may reverse this insensitivity to E2 and, particularly, to the synergistic effects of P in male rats of the Wistar strain. We examined whether this hormonal regimen would reverse this insensitivity in Sprague-Dawley rats. Gonadectomized animals received two injections of E2 (1 microgram per injection) 12 hr apart at 0900 and 2100 hr followed by P (0.5 mg) or oil, at 35 hr, and a mating behavior test, at 38 hr, subsequent to the initial E2 administration. This treatment was repeated four times at 4-day intervals. The inability of Sprague-Dawley male rats to respond to E2 and P was unaffected by this pattern of exposure to exogenous E2. Receptivity scores, lordosis quotients, and proceptivity were negligible in males, and significantly less than that displayed by females. In addition, the levels of sexual receptivity and proceptivity were facilitated by the availability of P following E2 in females, but not in males. The present findings fail to support a general hypothesis that "discontinuous" E2 stimulation, achieved by two spaced injections of this hormone, reverses developmental determinants of sex differences in responsiveness to hormones mediating female sexual behaviors.     

Sexual orientation, proceptivity, and receptivity in the male rat as a function of neonatal hormonal manipulation

The influence of neonatal androgen on the potential to exhibit feminine sexual behavior was investigated. Male rats castrated on Day 0 but not those castrated on Day 4 or later showed hop/darting, ear wiggling, and lordotic behavior in response to treatment with estrogen and progesterone in adulthood at a frequency equal to that of females. Neonatal treatment with testosterone propionate (1 mg/rat for 4 days) abolished the capacity to show these behaviors. In subsequent experiments, involving castration of male rats at 0 or 4 hr after cesarean delivery, the effect of the postnatal surge of testicular secretions on the expression of female sexual behavior was investigated. No differences were seen in the frequency of hop/darting, ear wiggling, and receptivity between males castrated immediately or 4 hr after delivery. In a preference test where the experimental male could choose between an estrous female and a sexually active male, the neonatally castrated males preferred the company of a male when treated with estrogen and progesterone. The implantation of testosterone resulted in a preference for an estrous female. It was concluded that testicular secretions in the newborn male influence adult sexual orientation and suppress the ability to show proceptive and receptive behaviors.     

Paced mating behavior in female rats in response to different hormone priming regimens

A female rat will display a repertoire of behaviors during a sexual encounter with a male rat including sexually receptive (the lordosis response) and proceptive (hopping, darting) behaviors. In addition, when given the opportunity, a sexually receptive female rat will approach and withdraw from the male rat, controlling the timing of the receipt of mounts, intromissions, and ejaculations, a behavior known as paced mating behavior. The present experiments tested the hypotheses (1) that progesterone regulates paced mating behavior, and (2) that multiple hormone regimens used previously to induce sexual receptivity have the same effect on paced mating behavior. Paced mating behavior was assessed in sexually receptive ovariectomized female rats after treatment with: (1) estradiol benzoate (EB; 30.0 mg/kg) followed by a range of doses of progesterone (P; 1.0-8.0 mg/kg), (2) two pulses of unesterified estradiol (E2; 2.0 microg/rat) followed by 1.0 mg/rat of P, and (3) EB alone (5.0 microg/rat) for 6 days. No differences in sexual receptivity or in paced mating behavior were observed across doses of P (1.0-8.0 mg/kg). In contrast, the number of hops and darts per min increased with the dose of P administered. E2 + P administration resulted in slightly, but significantly, lower levels of sexual receptivity along with significantly longer contact-return latencies following an intromission in relation to the other treatment conditions. In addition, female rats exhibited fewer hops and darts per min in response to E2 + P than in response to EB + 8.0 mg/kg of P. The administration of EB alone for 6 days induced levels of receptivity and paced mating behavior indistinguishable from EB + P, while eliciting significantly fewer hops and darts per min than the EB + 8.0 mg/kg P treatment condition. Hormone priming regimen had no effect on the percentage of exits displayed during the paced mating tests in any experimental phase. Dose of P had no effect on paced mating behavior in sexually receptive rats. In addition, P does not appear to be necessary for the display of paced mating behavior following long-term treatment with EB. In contrast, the pulsatile administration of E2 + P induced a different pattern of paced mating behavior in sexually receptive rats.     

The effects of estrogen and progesterone on female rat proceptive behavior

The relative importance of estrogen (EB) and progesterone (P) in stimulating proceptivity in ovariectomized female rats was studied. Proceptive behavior was measured quantitatively, providing a clear measure of response to experimental manipulation. When rats were tested biweekly after daily treatment with 0.4 μg/100 g body wt EB for 4 days, they showed maximal lordosis but low levels of proceptive behavior by the second test. Additional EB (3.0 μg/100 g body wt daily) failed to stimulate additional proceptivity. A graded increase in proceptive behavior resulted from administration of increasing doses of P (50, 100, 500 μg and 1.0 mg) to animals receiving EB priming as described above. The level of “soliciting” was significantly higher than EB-only-treated rats when 500 μg or 1.0 mg P was given. Ovariectomized, adrenalectomized rats, primed with 2.5 μg/100 g body wt EB daily for 7 days and tested on Day 8, were significantly less proceptive than ovariectomized, sham-adrenalectomized rats with the same hormone treatment. Four hours after injection of 1.0 mg P, there was no difference in proceptive or receptive behavior between sham- and adrenalectomized rats. It was concluded that if an EB dose is sufficient to induce maximal receptivity, additional estrogen does not stimulate proceptivity; unlike previous studies, the present data are not consistent with a global effect of ovarian steroids on both components of female behavior. Progesterone is more effective than estrogen in stimulating proceptive behavior, although proceptivity is not absolutely dependent on progesterone for expression. Proceptivity in EB-only-treated rats appears to be facilitated by adrenal P.     

Sustained influence of previous estradiol or testosterone treatments on sexual behaviors of female pigs

Two studies were conducted to determine the consequences of extended treatment with estradiol or testosterone on sexual behavior in postpubertal, female pigs. After ovariectomy, either steroid was administered for 6 weeks at dosages sufficient to maintain serum concentrations similar to those observed in mature male pigs. Behavioral evaluations were initiated 2 months after the last steroid treatment. These treatments reduced receptivity (immobile stance when placed with a mature male) and proceptivity (preference to remain near a mature male) in association with an increase in aggressive behavior. In females treated previously with both estradiol and progesterone, sexual behaviors 2 months later were similar to those of control females. When evaluations were repeated 5 months after extended estradiol treatment had ceased, receptivity and proceptivity had returned to that of control pigs and aggressive behavior had diminished greatly. Interpretation of these changes in behavior is that extended periods of estradiol or testosterone treatment sustain activational influences for a considerable amount of time after treatments cease and progesterone antagonizes estradiol's effect on these behaviors. In a companion study, pubertal and post-pubertal females were similar for receptivity but pubertal females spent less time near a mature male. This difference in proceptivity likely reflects a maturational change associated with sexual development in female pigs. Collectively, these observations in postpubertal, female pigs document that prolonged estrogen treatment will activate aggressive behaviors in association with reduced proceptivity and receptivity. Because these behavioral changes are reversible by 5 months after cessation of treatment, they are not the result of sexual differentiation.     

The phytoestrogen ferutinin improves sexual behavior in ovariectomized rats

The present study was designed to examine the effect of ferutinin chronic administration on sexual behavior of ovariectomized non-estrogen-primed rats. Starting from 3 weeks after ovariectomy, female rats were orally treated with ferutinin at the doses of 0.2 and 0.5 mg/kg, daily for 4 weeks. Ferutinin's effect was compared with that of estradiol benzoate, subcutaneously injected at the dose of 1.5 μg/rat twice a week. Animals were tested for sexual motivation, receptivity and proceptivity after 1, 2 and 3 weeks of treatment and for paced mating behavior after 4 weeks of treatment. Before each experimental test, they received progesterone injection (500 μg/rat).Both dosages of ferutinin significantly increased the receptive behavior in a time-dependent manner, as well as estradiol benzoate did. Also proceptive behaviors increased in ferutinin-treated animals in comparison with control ones. During the partner preference test ferutinin was able to induce a significant preference for a sexually active male over a sexually receptive female. Moreover, ferutinin restored a normal paced mating behavior, which had been suppressed by ovariectomy. These results show that ferutinin exerts an estrogenic activity in ovariectomized non-estrogen-primed female rats.     

Effects of progesterone implants in the habenula and midbrain on proceptive and receptive behavior in the female rat

Two brain areas behaviorally responsive to progesterone (P) were examined to determine their possible involvement in the control of rat preceptive behavior, i.e., solicitation behavior directed at the male. Progesterone implants were placed in the habenular nuclei and the interpeduncular nucleus-ventral tegmental area of the midbrain reticular formation (MRF). Different testing procedures and levels of priming with estradiol benzoate (EB) were used in order to distinguish the effects of P in either region on proceptive and receptive behavior during exposure to 10 mounts by stimulus males. To test for receptivity, sexually experienced 60-day-old ovariectomized (ovx) rats bearing stereotaxically placed guide cannulas extending to the habenula or MRF were given 10 μg EB subcutaneously. Forty-eight hours later, lordosis quotient (LQ) was determined. Immediately following this test, each animal was implanted with cholesterol (C) or P and was retested 2 hr later. Treatments for the proceptivity test were similar except that the animals received 2.5 μg EB/100 g body wt sc for 7 days before testing on the eighth day; LQ as well as hopping, darting, and ear wiggling were scored. In the receptivity test, P implantation in both the medial portions of the habenula and the MRF significantly increased lordosis above the levels found both in their preimplantation tests and following control implantation of C. Little proceptivity was observed. In the proceptivity test, P implants in both regions also significantly increased proceptive behavior above both types of control tests. All animals were highly receptive, and there was no difference in LQ among the groups. There was no increase of plasma P levels in similarly implanted animals during a 24-hr monitoring period, indicating that systemic leakage of the hormone was not responsible for the observed behavior. The data indicate that both the habenula and MRF are P-sensitive regions. Progesterone's action on the two areas facilitates expression of both proceptive and receptive components of female sexual behavior, indicating that the neural regulation of the two kinds of behavior is integrated at these levels.     

Hormonal control of proceptive and receptive sexual behavior and the preovulatory LH surge in the ewe: reassessment of the respective roles of estradiol, testosterone, and progesterone

When estrous behavior is induced in ovariectomized ewes by subjecting them to progestagen priming followed by a dose of estrogen large enough to guarantee estrus in all animals, an abnormally long period of estrus in induced, suggesting that the regime of steroid replacement needs modification. Using quantitative tests for proceptivity and receptivity, we studied the patterns of sexual behavior of intact ewes and then attempted to reproduce them in the same animals after they had been ovariectomized. We used various combinations of exogenous estrogen, androgen, and progestagen and compared the behavioral responses with an endocrine response, the preovulatory surge of luteinizing hormone (LH). In intact ewes, sexual behavior and the LH surge were closely synchronized and their characteristics differed slightly between the middle and the end of the breeding season. Proceptive behavior was not greatly affected by the frequency of tests, but the duration of receptivity was significantly reduced by frequent testing. In ovariectomized ewes, we found that: (a) progesterone priming is essential for normal patterns of receptive and proceptive behavior, and for synchronizing the behavioral and endocrine responses to estrogen; (b) androgens do not play a major role in the control of either receptive or proceptive behavior; and (c) the inclusion of a low dose of estrogen with the progestagen in the 'priming' regime improves the responses to estradiol-17 beta. Under these conditions, the timing, intensity and duration of the behavior are very close to those observed in the same ewes when they were intact and cycling spontaneously.     

Mu-, delta-, and kappa-opioid receptor agonists selectively modulate sexual behaviors in the female rat: differential dependence on progesterone.

Previous studies suggested that opioid receptor agonists infused into the lateral ventricles can inhibit (through mu receptors) or facilitate (through delta receptors) the lordosis behavior of ovariectomized (OVX) rats treated with estrogen and a low dose of progesterone. The present study investigated the behavioral and hormonal specificity of those effects using more selective opioid receptor agonists. Sexually experienced OVX rats were implanted stereotaxically with guide cannulae aimed at the right lateral ventricle. One group of rats was treated with estradiol benzoate (EB, 10 micrograms) 48 hr and progesterone (P, 250 micrograms) 4 hr before testing, whereas the other group was treated with EB alone. Rats were infused with different doses of the selective mu-receptor agonist DAMGO, the selective delta-receptor agonist DPDPE, or the selective kappa-receptor agonist U50-488. The females were placed with a sexually vigorous male in a bilevel chamber (Mendelson and Gorzalka, 1987) for three tests of sexual behavior, beginning 15, 30, and 60 min after each infusion. DAMGO reduced lordosis quotients and magnitudes significantly in rats treated with EB and P, but not in rats treated with EB alone. In contrast, DPDPE and U50-488H increased lordosis quotients and magnitudes significantly in both steroid-treatment groups. Surprisingly, measures of proceptivity, rejection responses, and level changes were not affected significantly by mu or kappa agonists, although proceptivity and rejection responses were affected by DPDPE treatment. These results suggest that the effects of lateral ventricular infusions of opioid receptor agonists on the sexual behavior of female rats are relatively specific to lordosis behavior. Moreover, the facilitation of lordosis behavior by delta- or kappa-receptor agonists is independent of progesterone treatment, whereas the inhibitory effect of mu-receptor agonists on lordosis behavior may require the presence of progesterone.     

Actions of RU 38486 on progesterone facilitation and sequential inhibition of rat estrous behavior: correlation with neural progestin receptor levels

The present study examined the actions of the antiprogestin RU 38486 on progesterone (P)-induced facilitation and sequential inhibition of estrous behavior and on brain cytosol progestin receptor (PR) levels in ovariectomized, estrogen-primed (0.5 micrograms of estradiol benzoate for 3 days) female rats. RU 38486 suppressed P-facilitated receptive and proceptive responses in a dose-dependent fashion when administered 1 hr prior to P. RU 38486 did not, however, block the sequential inhibitory effect of P. Indeed, when it was administered alone at a dose of 1 mg, animals were rendered behaviorally unresponsive to a P treatment 25 hr later. It is unclear whether RU 38486 is an agonist for P sequential inhibition of estrous behavior or if the apparent agonist action of RU 38486 actually results from a long-term antagonist effect. Estrogen-induced PRs remain elevated (35-55% above basal) in the hypothalamus (HYP) and preoptic area (POA) at 24 and 48 hr following the last estrogen injection. Thus P facilitation of estrous behavior is correlated with increased levels of cytosol PRs. RU 38486 reduced cytosol PRs in both brain regions to basal levels within 2 hr, and the levels remained suppressed 25 hr following the treatment. Hence there is a strong correlation between behavioral inhibition and suppressed cytosol PRs at both short (5 hr) and long (25 hr) intervals after RU 38486 administration. A P treatment which produced sequential inhibition of estrous responsiveness 24 hr later did not reduce the estrogen-induced level of cytosol PRs in either brain region. These results suggest that mechanisms in addition to induction of PRs may be necessary to ensure successful mating.     

Natural or hormone-induced sexual and social behaviors in the female brown lemming (Lemmus trimucronatus)

The behaviors of intact or ovariectomized, estradiol benzoate-treated or estradiol benzoate followed by progesterone-treated female brown lemmings were compared. Intact, diestrous females engaged in more social interactions with a male than did ovariectomized females (Experiment 1). In the first 5 min of a 1-hr mating exposure (Experiment 2, Test A) intact females in natural estrus engaged in more social and sexual behaviors than did ovariectomized females in estrogen-induced estrus. However, during the last 5 min of the 1-hr exposure (Test B) ovariectomized females receiving estrogen alone continued to show high levels of sexual activity with a male partner, while intact estrous females or females receiving estrogen followed by progesterone showed an apparent drop in sexual receptivity and an increase in aggressivity. Aggressive behaviors, as indexed by threat-leap behaviors on the part of the female may increase in the presence of progesterone. Declines in sexual activity, occurring within 1 hr of progesterone injection, were apparently dependent on the interaction of progesterone and copulatory events which may affect both the male and female.     

Progesterone versus estrogen facilitation of female sexual behavior by intracranial administration to female rats

The CNS sites of action for progesterone facilitation of female sexual behavior are disputed. Among the areas most often cited are the ventromedial hypothalamus and the ventral midbrain. There is also a controversy about whether estradiol may substitute for progesterone for the facilitation of receptive behavior when given systemically or intracranially. We tested VMH and ventral midbrain applications of estradiol versus progesterone for the facilitation of female sexual behavior in estrogen-primed, ovariectomized female rats. Subjects were implanted with bilateral guide tubes aimed at ventral hypothalamic or midbrain sites. Estrogen-primed rats received either 28-gauge insert cannulae filled at the lumen with pure progesterone, estradiol, or cholesterol, or empty tubes, and were tested for receptivity with intact, experienced stud males just before, and 1 and 4 hr after, intracranial hormone administration. Significant estrous responsiveness was seen only in the 4-hr test after progesterone was implanted in the VMN in the first intracranial cannula test. We conclude, in contrast to some previous reports, that administration of progesterone to the VMN is more effective in the facilitation of female sexual behavior than when it is implanted in the ventral midbrain, and that administration of estradiol to either site is ineffective.     

Systemic ICI 182,780 alters the display of sexual behaviors in the female rat

The present study investigates the effects of the antiestrogen ICI 182,780 (ICI) on the display of sexual behaviors in female rats. ICI 182,780 is a pure anti-estrogen and when given systemically, ICI is thought to act only in the periphery, and is not believed to cross the blood brain barrier. The present study examines the effects of ICI on sexual receptivity and on paced mating behavior following treatment with estradiol benzoate (EB) and progesterone (P) (Experiment 1) or with EB alone (Experiment 2). In Experiment 1, ICI (250.0 microg) did not affect the display of receptivity or paced mating behavior induced by EB and P. In contrast, in Experiment 2 female rats receiving EB alone displayed a decrease in the level of sexual receptivity following treatment with 500.0 and 750.0 microg ICI (but not 250.0 microg ICI). In addition, in Experiment 2 EB-treated female rats receiving 250.0 microg ICI spent more time away from the male rat following an intromission and were more likely to exit from the male compartment following a mount. Last, ICI had potent antiestrogenic effects on vaginal cytology (Experiment 2) and on the uterus (Experiments 1 and 2). The present study supports a role for peripheral estrogen receptors in sexual receptivity and paced mating behavior and suggests that estrogen receptor activation may decrease the aversive sensation associated with sexual stimulation.     

Sexual receptivity in hamsters: brain nuclear estrogen and cytosolic progestin receptors after single and multiple steroid treatments and during the estrous cycle

This series of experiments investigated the relationship between various treatments consisting of estradiol benzoate (EB) and progesterone (P) on sexual receptivity and on concentrations of nuclear estrogen receptors (NER) and cytosolic progestin receptors (CPR) in the hypothalamus-preoptic area in female hamsters. The injection of 1 microgram EB at 0 and 24 hr resulted in higher levels of receptivity (after 0.25 or 0.5 mg P), NER and CPR compared to those obtained after a single injection of 2 micrograms EB. Animals treated with 5 micrograms EB at 0 and 24 hr displayed greater levels of receptivity (after 0.5 mg P) and had higher NER concentrations than animals given a single injection of 10 micrograms EB. Groups treated with either 1 microgram EB at 0 hr or 0.5 microgram EB at 0 and 24 hr did not differ and showed low levels of receptivity, NER and CPR, NER and CPR were also measured on each day of the estrous cycle. NER levels rose between Days 1 and 2, again between Days 2 and 3, and remained elevated on Day 4. CPR levels increased between Days 2 and 3, and there was no difference between Days 3 and 4. Taken together, these data suggest that receptivity in hamsters after estrogen exposure is correlated with the accumulation and maintenance of relatively high NER levels and on the induction of CPR. This can be accomplished by a single large injection of EB or by smaller split doses.     

Facilitation of receptive behavior in estrogen-primed female rats by the anti-progestin, RU 486

The progestin receptor antagonist RU 38486 (henceforth referred to as RU 486) was tested for facilitative effects on female receptive behavior in ovariectomized Long-Evans rats primed with 2 micrograms estradiol benzoate (EB). RU 486 (0, 0.5, 1.6, or 5.0 mg) was administered 48 hr after estrogen priming. The lordosis quotient (LQ) and lordosis score (LS) were assessed 4 hr after RU 486 administration in a standardized test consisting of a 10-mount test by a stimulus male. A significant dose effect was found by both LQ and LS, with those subjects receiving 5 mg of RU 486 being significantly more receptive than vehicle control animals. Thus RU 486 acted as a weak progestin agonist under testing conditions typical for assessment of progestin facilitation of female sexual behavior in rats. Low levels of proceptive behavior (hops and darts) were seen in a minority of the tests, and did not vary systematically as a function of the dose of RU 486 administered. We also examined the effects of RU 486 given before progesterone (P) on receptivity in a blocking paradigm and confirmed previous reports that the antagonist significantly attenuates facilitation of sexual behavior when given in combination with P. A progestin receptor assay of the cytosols of the hypothalamus-preoptic area in estrogen-primed female rats treated with 5 mg RU 486 revealed a significantly greater depletion of available cytosolic P receptors than when rats were treated with a similarly facilitating dose of P (100 micrograms). The results suggest a possible dual mode of action for RU 486--a weak, receptor-mediated agonistic effect on sexual behavior when given alone to estrogen-primed rats, and a competitive blocking effect on receptivity when administered with P.     

Expression of adult female patterns of sexual behavior by male, female, and pseudohermaphroditic female rhesus monkeys

Gonadally intact pseudohermaphroditic female and normal female and neonatally castrated male rhesus monkeys were given estrogen treatment as adults and evaluated for attractivity, proceptivity, and receptivity during tests with a tethered stud male. Pseudohermaphrodites were produced by injecting their mothers during pregnancy with either testosterone propionate (TP) or dihydrotestosterone propionate (DHTP). Castrated males had reliably lower attractivity than normal females on all indicator responses shown by the tethered males. Additionally, castrated males showed reliably fewer proceptive responses on 4 of 5 measures than normal females. Receptivity could not be assessed in this situation for castrated males, because tethered males never contacted them unless the castrated males were displaying presentation. No reliable differences were observed between pseudohermaphrodites produced by prenatal treatments with TP or DHTP. Pseudohermaphrodites generally showed reliably less attractivity and proceptivity than normal females and reliably more of these traits than castrated males. Attractivity scores for pseudohermaphrodites were not different from those for normal females until proximity to the tethered male was established. Receptivity was not different in pseudohermaphrodites compared with normal females. Results indicate prenatal androgenization and its developmental sequelae lead to a defeminization in adulthood which, in this testing situation, was principally manifested by a deficiency in the performance of proceptive behaviors. Additionally, defeminization in rhesus monkeys, unlike that demonstrated in rodents, does not depend upon actions of an aromatizable androgen.