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.     

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.     

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.     

Different doses of estradiol benzoate induce conditioned place preference after paced mating

The ovarian hormones estrogen and progesterone are required for the complete display of sexual behavior in female rats. Paced mating produces a reward state in intact cycling and ovariectomized (OVX), hormonally primed females as evaluated by the conditioned place preference (CPP) paradigm. Most of the studies that have evaluated CPP induced by paced mating in OVX females have used relatively high doses of estradiol benzoate (EB). In the present study we determined if different doses of EB, combined with progesterone (P), could induce CPP after paced mating. For this purpose OVX female rats were divided in five groups that received one of different doses of estradiol benzoate (5, 2.5, 1.25 or 0.625 μg estradiol + 0.5 mg of progesterone) before being allowed to pace the sexual interaction and conditioned in a CPP paradigm. We found that the lowest dose of EB used (0.625 μg) significantly reduced the lordosis quotient and the lordosis coefficient. Even though these females paced the sexual interaction, they didn't change its original preference, suggesting that sexual interaction did not induce a positive affective, reward state. Females allowed to pace the sexual interaction with higher doses of EB developed CPP after paced mating. These results indicate that a threshold of estradiol is required for paced mating to induce CPP.     

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.     

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.     

Neonatal hormonal influences on the development of proceptive and receptive feminine sexual behavior in rats

The objective of this study was to examine the influence of androgen and of the inhibiting of aromatization of androgen to estrogen during the early neonatal period on the development of receptive (lordosis and acceptance of stimulus male mounting attempts) and proceptive (affiliation with and solicitation of stimulus males) feminine sexual behavior. Within 8 hr of birth, male rats were castrated or received subcutaneous implants of the aromatase inhibitor androst-1,4,6-triene-3, 17-dione (ATD) while females received injections of testosterone propionate (TP). At 90 days of age all treated animals and controls were tested for receptive and proceptive feminine sexual behavior. It was found that androgen present neonatally blocked proceptive as well as receptive behavior patterns in adult rats. The proceptive and receptive feminine sexual behavior patterns displayed by adult males deprived of the effects of androgen neonatally either by castration or by treatment with ATD were comparable to those of normal females.     

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.     

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.     

Regulation of estrogen-stimulated lordosis behavior and hypothalamic progestin receptor induction by antiestrogens in female rats

Two estrogen antagonists, CI-628 (CI) and tamoxifen (TX), were used to examine the relationship between estrogen priming of lordosis behavior and progestin receptor induction in the hypothalamus-preoptic area (HPOA) of ovariectomized female rats. Lordosis behavior was assessed by measuring lordosis quotients (LQ) in response to injection of 2 micrograms of estradiol benzoate (EB) followed 48 hr later by 500 micrograms of progesterone (P). Behavior testing began 4 hr after P injection. The effects of antiestrogens were assessed by injecting CI and TX (1-2 mg) from 0 to 48 hr prior to EB. Levels of cytosol progestin receptor in the HPOA were determined by quantifying the specific binding of 0.5 nM [3H]R5020 to cytosols from animals receiving the same EB and antiestrogen treatments used in behavioral testing. TX given concurrently with or CI given 2 hr before EB abolished both lordosis behavior and induction of HPOA progestin receptors. In contrast, CI given 12 hr prior to EB abolished lordosis but permitted a 95% elevation in the concentration of progestin binding sites in the HPOA. TX or CI given 48 hr before EB resulted in moderate levels of lordosis (mean LQs from 56 to 69) and induction of HPOA progestin receptors from 85 to 130% above noninjected controls. However, CI given 24 hr prior to EB produced less than a 40% increase in brain R5020 binding even though lordosis behavior was equivalent to that seen in the 48-hr animals (mean LQ = 53). These data indicate that the effects of antiestrogens on female sexual behavior and on the synthesis of brain progestin receptors depend on which antiestrogen is used and the time interval between administration of estrogen and antiestrogen. They also demonstrate that under some conditions estrogen induction of cytosol progestin receptors in the HPOA can be dissociated from estrogen priming of lordosis behavior in rats.     

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.     

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.     

Specificity and neural sites of action of anisomycin in the reduction or facilitation of female sexual behavior in rats

These experiments were designed to investigate the role of neuronal protein synthesis in the hormonal activation of female sexual behavior using intracranial implants of the protein synthesis inhibitor, anisomycin. In the first experiment, female rats receiving bilateral cannulae implants in the medial preoptic area (POA), septal region (SEPT), ventromedial hypothalamus (VMH), or midbrain central gray (CG) were injected with 2.5 micrograms estradiol benzoate (EB), followed 48 hr later by 500 micrograms progesterone (P). Females receiving anisomycin in the VMH at the time of EB injection had lower levels of lordosis and darting compared to tests without anisomycin. Sexual behavior was unaffected in females receiving anisomycin implants in the POA, SEPT, or CG. In a second experiment, we replicated the finding that anisomycin could attenuate lordotic responsivity when placed in the VMH of female rats injected with 2.5 micrograms EB and 500 micrograms P. In addition, we found that POA implants of anisomycin could facilitate lordosis in females given a low dose of EB (1.25 microgram) plus 500 micrograms P. In a third experiment, we assessed the effects of anisomycin application to the VMH or POA of female rats receiving estradiol (E; diluted 1:250 with cholesterol) implants in the VMH and systemic P. Treatment of the VMH with anisomycin prior to E in the VMH suppressed lordotic responding, whereas anisomycin application to the POA prior to E in the VMH had no effect on lordosis. The results of these experiments suggest that reducing protein synthesis in the region of the VMH disrupts the action of estrogen on the VMH, and that the facilitative action of anisomycin in the POA of female rats requires more estrogen treatment than threshold stimulation of the VMH alone.     

The display of sexual behaviors by female rats administered ICI 182,780

ICI 182,780 (ICI) is a pure antiestrogen that when administered systemically does not cross the blood-brain barrier, thus its actions are limited to the periphery. Four experiments were conducted to test the effects of ICI on the display of sexual behaviors in ovariectomized rats. Experiment 1 examined the effects of three doses of ICI (250, 500, and 750 μg/rat) on sexual receptivity and paced mating behavior in rats primed with estradiol benzoate (EB) in combination with progesterone (P). Experiments 2 and 3 compared the display of sexual behaviors in rats primed with EB+P or EB alone and administered either 250 μg ICI (Experiment 2) or 500 μg ICI (Experiment 3). Experiment 4 tested the effects of ICI (250 and 500 μg) on the expression of estrogen-induced progestin receptors in the uterus. ICI did not affect the display of sexual receptivity in any experiment. In rats primed with EB+P, paced mating behavior was altered by the 500 and 750 μg, but not the 250 μg, doses of ICI. The lowest (250 μg) dose of ICI did alter paced mating behavior in rats primed with EB alone. The effects of ICI on paced mating behavior were manifested by a substantial lengthening of contact-return latencies following intromissions and ejaculations. The percentage of exits were not affected by ICI. Estrogen stimulation of uterine weight and induction of uterine progestin receptors was suppressed by ICI (250 and 500 μg). ICI effects on paced mating behavior in hormone-primed female rats are likely to reflect antiestrogenic actions in the periphery, including interference with the estrogen induction of progestin receptors.     

Estrogenic contributions to sexual differentiation in the female guinea pig: influences of diethylstilbestrol and tamoxifen on neural, behavioral, and ovarian development

We administered the synthetic estrogen, diethylstilbestrol (DES), or the antiestrogen, tamoxifen, to pregnant guinea pigs and observed the consequences for sexual differentiation of their female offspring. Hormones were administered during the period when treatment of fetuses with testosterone influences the development of sex-related traits (approximately Days 30 to 65 of gestation). Ovarian function, masculine and feminine sexual behavior, and the structure of a sexually dimorphic neural region in the preoptic area were assessed in adulthood in hormone-exposed animals and in oil-treated and untreated controls. Prenatal exposure to DES dipropionate (DESDP) caused masculinization and defeminization. DESDP-treated females mounted more than control females, both without hormonal stimulation and when given testosterone propionate (TP) as adults. The sexually dimorphic neural region was also masculinized in these females. In regard to defeminization, they showed delayed vaginal opening, impaired progesterone (P) production, an absence of corpora lutea, and impaired lordosis and mounting responses to estradiol benzoate (EB) and P. Prenatal treatment with tamoxifen produced a complicated pattern of results. Tamoxifen-exposed females evidenced less masculine-typical behavior, showing diminished mounting without hormonal stimulation and in response to TP. However, they also showed delayed vaginal opening, enhanced P production, and impaired mounting in response to EB and P. Their lordosis behavior and the volume of the sexually dimorphic neural region were unaffected. These results suggest that estrogens play a substantial role in sexual differentiation in the guinea pig. High levels of estrogen promote masculine-typical development, and unusually low levels may impair some aspects of both masculine-typical and feminine-typical development.     

The reversible inhibition of steroid-induced sexual behavior by intracranial cycloheximide

Cycloheximide(Cyclo), an inhibitor of protein synthesis by a direct action on protein synthesis at the ribosomal level, was used to reversibly inhibit estrogen-induced sexual receptivity. Cyclo (100 μg per rat) was infused into the preoptic area(POA) of ovariectomized rats at varying times before, simultaneously with, and after 3 μg of subcutaneous estradiol benzoate (EB). All animals received 0.5 mg progesterone (P) 36 hr after EB, and were tested for sexual receptivity 4–6 hr after P. The females were placed with stud males and a lordosis quotient was computed for each female (lordosis quotient = number of lordosis responses/20 mounts by the male × 100). Females receiving Cyclo 6 hr before, simultaneously with, or 12 hr after EB showed significantly lower levels of sexual receptivity when compared to females receiving Cyclo 36 hr before and 18 and 24 hr after EB. When those animals that showed low levels of sexual behavior after Cyclo infusion were reprimed with EB and P 7 days later and presented with a male they showed high levels of sexual receptivity. Thus, the effect of Cyclo was reversible. Only Cyclo infusions into the POA (bilateral) and third ventricle were effective in suppressing sexual behavior. Caudate nucleus, lateral ventricle, and unilateral POA infusions were without effect.The data presented are in agreement with earlier work that utilized actinomycin D to inhibit steroid-induced sexual behavior. Cyclo was found to be less toxic than actinomycin D. All of the available evidence is consistent with the hypothesis that estrogen stimulates RNA and/or protein synthesis in its facilitation of sexual behavior in the female rat.     

Blockade of lordosis by androst-1,4,6-triene-3,17-dione (ATD) and tamoxifen in female hamsters primed with testosterone propionate

Normal female hamsters display lordosis after testosterone propionate (TP) plus progesterone (P) treatments. Such effect is probably mediated through aromatization of testosterone (T) into estradiol. If so, then an aromatase inhibitor (ATD) or an estrogen antagonist (tamoxifen, TAM) should be able to block the activational effect of T on lordosis. To test this hypothesis, 48 ovariectomized female hamsters were assigned into six groups which, according to treatments received, were ATD + TP, TAM + TP, OIL + TP, ATD + EB (estradiol benzoate), TAM + EB, and OIL + EB groups. The groups received assigned treatments for 2 days and were injected with P on the third day. Five minutes of behavior test was conducted 4 hr after P injection. The OIL + TP, OIL + EB, and ATD + EB groups all had averaged total lordosis duration (TLD) longer than 200 sec. The TLD of the TAM + EB group was only 117 sec. The ATD + TP and TAM + TP groups showed almost no lordosis. The results showed that the estrogen antagonist (TAM) impaired lordosis no matter whether the animals were primed with TP or EB, but the aromatase inhibitor (ATD) blocked lordosis only in TP primed females. It is concluded that the aromatization of T to estrogen is required for testosterone activation of lordosis in female hamsters.     

Effects of septal lesions on behavioral sensitivity of female rats to gonadal hormones

Spayed female rats were given bilateral septal lesions or a sham operation and 3 wk later tested for hormone-induced female sexual behavior. When primed with 0.5, 1.0, or 2.0 μg of estradiol benzoate (EB) per day for 3 days and tested for lordosis behavior on the fourth day, animals with septal lesions showed a positive dose-related increase in mean lordosis quotient (LQ), whereas control animals showed a low mean LQ for all doses of EB. After priming with a low dose of EB (0.5 μg/day for 3 days), progesterone administration prior to behavior testing on day 4 produced a comparable facilitation in LQ for both septal-lesioned and sham-operated animals. When treated for 3 days with either 50 or 150 μg of testosterone propionate (TP) and given progesterone prior to behavior testing on day 4, female rats with septal lesions showed a higher mean LQ than sham-operated rats. Thus, septal lesions increase the behavioral sensitivity of female rats to both EB and TP as measured by female sexual behavior, but do not appear to alter the responsiveness of animals to progesterone.     

Effects of naloxone and naltrexone on receptive and proceptive behaviors in female rats.

The sexual receptive and proceptive behaviors induced by opiate antagonists, naloxone and naltrexone in estrogen-primed ovariectomized rats were observed under the presence of sexually active males. The females were treated intraperitoneally with naloxone or naltrexone at doses ranging from 0.5 to 4.0 mg/kg and the sexual behavior of females was tested before and after the injection of drug. The results obtained suggest that the opiate antagonists play a role in the regulation of lordosis behavior, but not proceptive behavior in female rats.