Role of septum and preoptic area in regulating masculine and feminine sexual behavior in male rats

The effects of septal or preoptic lesions on both masculine and feminine sexual behaviors were examined in castrated adult male rats. Three weeks after brain surgery, animals were implanted with Silastic tubes containing testosterone (T) and observations of masculine sexual behavior were carried out four times every 5 days. T tubes were removed immediately after the end of the masculine behavioral tests. Two weeks later, animals implanted with Silastic tubes containing estradiol-17 beta(E2) were subjected to three feminine sexual behavioral tests at 5-day intervals. The bilateral lateral septal lesion (LSL) and the medial preoptic lesion (MPOL) effectively suppressed the performance of mounts, intromissions, and ejaculations, whereas the medial septal lesion (MSL), the dorsolateral preoptic lesion (DPOL), and the sham operation did not show any significant suppression of these behaviors. In the feminine sexual behavioral tests, intact and sham-operated control males showed only a low lordotic activity. However, the performance of the lordosis reflex was markedly facilitated by LSL or DPOL, while the lordotic activity of MSL and MPOL males was not significantly different from that of control males. These results suggest that the lateral septum exerts not only a facilitatory influence on masculine sexual behavior but also an inhibitory influence on feminine sexual behavior in male rats. On the other hand, the medial preoptic area may play a critical role in regulating masculine sexual behavior in male rats.     

Effects of neonatal septal lesions on reproductive behavior of male and female rats

The purpose of this study was to examine the effects of neonatally placed septal lesions (SL) in male, female, and androgenized female rats on reproductive behavior. Animals were castrated as adults and tested for both feminine and masculine sexual behavior. After treatment with estradiol benzoate (EB) alone (2 μg daily for 3 days), only the females with SL which had not been given testosterone propionate (TP) neonatally showed a facilitation of lordosis behavior. Following EB (2 μg for 3 days) plus 0.5 mg progesterone (P), both the lesioned and the sham-operated female groups showed an increase in the display of lordosis in either hormonal condition. All animals were given a pretest for masculine sexual behavior and tested on Days 4, 7, 11, and 15 of daily TP treatment (150 μg/day). There was no effect of the neonatally placed SL on masculine sexual behavior in female rats or in female rats androgenized with 30 μg TP. However, lesioned females treated neonatally with 1 mg TP showed a marginal enhancement of masculine sexual behavior. Male rats given SL neonatally showed a marked enhancement of masculine sexual behavior compared to that of controls. These results suggest that, depending on the neonatal hormone environment, SL selectively increase behavioral sensitivity to hormones. Although neonatally lesioned females show behavioral responses similar to females given SL as adults, male rats given SL neonatally are unique in that they show enhanced masculine sexual behavior whereas males lesioned as adults do not.     

Independence of the differentiation of masculine and feminine sexual behavior in rats.

Male rats received Silastic implants of the aromatase inhibitor, 1,4,6-androstatriene-3, 17-dione (ATD), on days 2–10 of life. Controls received blank implants. There were no differences in the masculine sexual behavior of ATD and control males when they were tested as gonadally intact adults. In contrast, even without exogenous hormone treatment, nine of 14 ATD males exhibited lordosis behavior, whereas only one of 12 controls did so. In addition, during a sexual preference test in which access was provided to both a sexually receptive female and to a stud male, there was no difference in the proportions of ATD ($\text{11}\text{14}$) and control ($\text{7}\text{12}$) males that copulated with the stimulus female; however, seven of the ATD males also exhibited feminine sexual behavior including some instances of solicitation. Only one of the control males showed any lordosis behavior. In general, all animals spent more time with the stimulus female than with the stud male. At the termination of preference testing, all animals were castrated and then tested twice for feminine sexual behavior under exogenous estradiol benzoate and progesterone. All of the ATD males showed lordosis behavior with a mean lordosis quotient (LQ) of 85; and 11 of the 14 also showed solicitation behavior. Only five of 12 control males exhibited lordosis ($\text{X}\text{?}\text{LQ}\text{= 59}$) and only one showed solicitation behavior. These results indicate that the propensity of males to show feminine sexual behavior can be manipulated independently of the capacity for masculine sexual behavior. Moreover, our results suggest that the process of defeminization may occur primarily postnatally in rats since treatment during that period results in substantial increments in later feminine sexual behavior including solicitation behaviors.     

Postnatal treatment of rats with adrenergic receptor agonists or antagonists influences differentiation of sexual behavior

The aim of the study was to investigate the possible role of the adrenergic system in development and differentiation of neural centers controlling sexual behavior in adulthood. For this purpose normal and androgenized female rats were treated with the alpha 1-receptor antagonist prazosin, the alpha 2-receptor agonist clonidine, or the alpha 2-receptor antagonist yohimbine-HCl throughout the first week of life. In adulthood all animals were ovariectomized and, after appropriate hormone-priming, they were tested for the capacity to display female and male sexual behavior patterns. Alteration of adrenergic transmission during the critical postnatal period for sexual differentiation of neural centers resulted in significant changes in the capacity to express female lordosis behavior in adulthood. In nonandrogenized animals clonidine significantly reduced the capacity for lordosis behavior. In androgenized animals clonidine had the opposite effect; it attenuated the inhibitory effect of testosterone propionate (TP) on differentiation of lordosis behavior. Prazosin, which was without effect in nonandrogenized animals, also attenuated the inhibitory effect of TP on differentiation of lordosis behavior. Yohimbine was without effect in androgenized and nonandrogenized animals. There was no influence of any of the adrenergic drugs on differentiation of male sexual behavior. In conclusion, differentiation of lordosis behavior seems to be mediated or modulated via adrenergic transmission. The defeminizing effect of testosterone postnatally on the differentiation of lordosis behavior seems to be expressed via alpha 1-adrenergic transmission, and diminished adrenergic activity during the postnatal period seems to protect the developing brain against this effect of testosterone.     

Appetitive and consummatory sexual behaviors of female rats in bilevel chambers. II. Patterns of estrus termination following vaginocervical stimulation

Copulation with intromission or manual vaginocervical stimulation (VCS) shortens the duration that intact female rats maintain lordosis responding during estrus. The present study examined whether VCS could shorten the duration of both appetitive and consummatory measures of female sexual behavior, and whether these effects occur differentially in time and across different hormone priming intervals. Ovariectomized, sexually experienced female rats were administered subcutaneous injections of estradiol benzoate 48 h and progesterone 4 h, before receiving 50 manual VCSs with a lubricated glass rod distributed over 1 h. Control females received sham VCSs distributed over the same time. The females were then tested for sexual behavior in bilevel chambers with two sexually vigorous males (to one ejaculatory series or 10 min with each male, separated by 5 min) 12, 16, and 20 h after VCS. Prior to the final hormone treatment, different groups of females had been given the same hormone treatment either 28, 14, 7, or 4 days before. In females tested at 28- and 14-day hormone intervals, VCS induced both active and passive rejection responses at 12, 16, and 20 h. In contrast, females that received sham VCS displayed relatively normal sexual behavior at 12 h, although by 16 and 20 h these females displayed active and passive rejection. Females tested at 7- or 4-day intervals displayed normal levels of lordosis at all testing times, regardless of VCS treatment. These data indicate that VCS facilitates rejection responses that precede the decrease in lordosis responsiveness. However, the effects of VCS are dependent on the frequency of hormone priming, suggesting that hormone treatment may block some of the long-term inhibitory effects of VCS on female sexual behavior.     

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.     

Differential effects of the anti-estrogen MER-25 and of three 5alpha-reduced androgens on mounting and lordosis behavior in the rat.

Four experiments were performed in order to evaluate further the hypothesis that androgen must be aromatized to estrogen for the activation of masculine sexual behavior in the male rat. In Experiment 1 it was found that the anti-estrogen MER-25 failed to disrupt mounting behavior in castrated males which simultaneously received testosterone propionate (TP). However, in Experiment 2 it was found that MER-25 as weil as 3β-androstanediol effectively activated masculine behavior in castrated males treated simultaneously with dihydrotestosterone propionate. Both MER-25 and 3β-androstanediol had previously been shown to display an affinity for cytoplasmic estradiol-17β receptors present in male rat anterior hypothalamus. In Experiments 3 and 4, performed with ovariectomized females, it was found that whereas MER-25 antagonized the stimulatory effect of estradiol benzoate (EB) on lordosis behavior, 3β-androstanediol did not. In addition, 5α-dihydrotestosterone and 3α-androstanediol, two compounds which had previously been shown to have almost no affinity for estradiol-17β receptors in the hypothalamus, both inhibited the stimulatory effect of EB on lordosis. It is concluded that the fact that anti-estrogens suppress lordosis induced in females with either EB or TP, but fail to disrupt TP-induced mounting behavior in male rats does not argue against the aromatization hypothesis for masculine sexual behavior.     

Lordosis behavior in male rats after lesions in different regions of the corticomedial amygdaloid nucleus

The aim of the experiment was to study the effects of stereotaxic lesions of the anterior and the posterior regions of the corticomedial amygdaloid nucleus (CMN) on the display of lordosis behavior by the male rat. Animals were orchidectomized as adults and given estradiol benzoate and progesterone (P) sequentially. Sexual behavior testing was performed by 9 +/- 1 hr after P injection. Lesions placed into the posterior region of the CMN significantly decreased the proportion of animals showing lordosis behavior as compared to sham-operated and control animals. By contrast lesions in the anterior region of the CMN did not cause any changes in the proportion of animals displaying lordosis but markedly increased the lordosis quotient (LQ) of responding animals. The CMN was then concluded to exert a dual control in the display of lordosis behavior in the male rat with a posterior region regulating the willingness of animals to display lordosis behavior and rostral region subserving inhibitory mechanisms related to the sexual performance (LQ values).     

Induction of progestin receptors in the mediobasal hypothalamus of gonadally intact male rats primed with estrogen in relation to display of lordosis behavior

The purpose of this study was to determine whether the effects of estrogen on lordosis behavior in the male rat were related to the number of progesterone (P) receptors in the mediobasal hypothalamus (MBH) and/or dependent on blood P concentration. Two groups of gonadally intact male rats were given five successive doses of 1.0 or 2.5 micrograms estradiol benzoate (EB) and tested for lordosis behavior with a male stimulus at the end of the treatment. One month later they were again injected with EB and sacrificed under the same temporal schedule, but they were not tested for lordosis so as to prevent any emotionally stressful effects of intermale cohabitation. The males given 2.5 micrograms EB more frequently displayed lordosis responses to male mounts than those receiving 1 microgram EB, with a parallel increase in the number of MBH P receptors. The total number of MBH P receptors also appeared to be higher in the animals that displayed lordosis responses (lordosis group) than in those which did not (no lordosis group). In contrast, the display of lordosis behavior was negatively correlated with blood P concentration. Comparing MBH P receptors and blood P values in the EB treated and in nonhormonally treated gonadally intact animals which had been selected for either ability or inability to spontaneously display lordosis behavior, we observed that (1) EB was capable of increasing the number of MBH P receptors in the male rat; and (2) in the absence of EB treatment blood P values were higher in the animals showing lordosis than in those which did not. These data are discussed with respect to observations made in castrated male rats and in ovariectomized females.     

Lordosis behavior in intact male rats: effects of hormonal treatment and/or manipulation of the olfactory system

The aim of this study was to investigate the olfactory mechanisms regulating the display of lordosis behavior in intact Wistar male rats bred in our colony. Gonadally intact males show a low capacity to respond by lordosis to male mounts and were insensitive to manipulations of the olfactory system (exposure to the odor of male urine or accessory bulb removal (AOBR)) which have been previously shown to facilitate the display of lordosis behavior in orchidectomized animals primed with ovarian hormones. Treatment with either estradiol benzoate (EB) or EB and progesterone (P) consecutively did not render these gonadally intact animals sensitive to the effects of AOBR. By contrast exposure to male urine was capable of facilitating the display of lordosis behavior in intact male rats given EB + P consecutively. These results are discussed in the light of previous findings showing that (1) two inhibitory structures, the accessory olfactory bulb and the septal and preoptic areas, are involved in the control of lordosis behavior in the male rat; (2) the effects of olfactory cues on the display of lordosis behavior are dependent on the action of both EB and P in orchidectomized animals.     

Intracranial dialysis and microinfusion studies suggest that morphine may act in the ventromedial hypothalamus to inhibit female rat sexual behavior.

The present investigation examined the neural sites and mechanisms of opiate inhibition of female sexual behavior. Systemic administration of morphine (10 mg/kg) significantly reduced ovarian steroid-induced estrous behavior in female rats. This behavioral inhibition was prevented when the opiate receptor antagonist naloxone (5 mg/kg) was administered 30 min prior to morphine. Bilateral infusion of morphine directly into the ventromedial hypothalamus (VMH) also inhibited hormone-dependent estrous behavior for at least 2 hr. Furthermore, naloxone infusion into the VMH 20 min before behavior testing reduced the inhibitory effects of systemically administered morphine on lordosis. These results suggest that morphine may inhibit female sexual behavior by acting directly on the VMH, the primary site at which ovarian steroids facilitate this behavior. In a separate experiment we used in vivo brain microdialysis to test the hypothesis that morphine inhibits lordosis by interfering with norepinephrine (NE) neurotransmission in the VMH. In control rats, the onset of mating was associated with increased NE release in the VMH. Morphine-treated animals displayed neither behavioral estrus nor elevated NE release from the VMH when tested with stimulus males. These data are consistent with the hypothesis that morphine suppresses NE release in the VMH. Nevertheless, mechanisms other than or in addition to attenuation of hypothalamic NE release may contribute to the inhibitory effects of morphine on lordosis.     

Effects of voluntary and forced exercise on lordosis behavior in female rats

We measured sexual behavior (lordosis) in ovariectomized, steroid-treated, exercising female rats. When estradiol-treated animals exercised voluntarily, lordosis was directly related to the amount of exercise. Forced exercise (swimming) following treatment with estradiol 17 beta and progesterone significantly increased lordosis scores but only after animals swam for 2.5 hr per day. Lordosis behavior returned to baseline levels 7 weeks after forced exercise was stopped. Circulating levels of estrogen and progesterone measured immediately after behavioral testing did not differ between animals forced to exercise and their controls. The mechanisms responsible for the increase in lordosis behavior following exercise are unclear. It is possible that a change in body composition, a change in neural sensitivity to gonadal steroids, and/or changes in pituitary or adrenal function contribute to the increased lordosis behavior in exercised animals.     

Differential effects of two estrogen antagonists on the development of masculine and feminine sexual behavior in hamsters

To determine whether nonsteroidal antiestrogens can be used to investigate the role of aromatization in behavioral masculinization and defeminization, newborn male and female hamsters were administered 0.5 or 5.0 μg of the antiestrogens nafoxidine or tamoxifen on postnatal Days 1 and 2. Other females received 1.0 μg of the synthetic estrogen RU-2858 (RU) alone or in combination with 0.5 or 5.0 μg of nafoxidine or tamoxifen. All animals were tested for the display of masculine and feminine sexual behaviors in adulthood. Nafoxidine, tamoxifen, and RU all reduced lordosis behavior in adult females, indicating that the antiestrogens probably have some estrogenic properties. Nafoxidine had no effect on male mating behavior in female hamsters when given alone; when given to male hamsters or female hamsters receiving a partially masculinizing dose of RU, this compound effectively reduced the frequencies of masculine sexual behaviors (mounts and intromissions) displayed by the treated animals. However, nafoxidine-treated males had the same mating efficiency (ME = intromissions/ mounts) as control males. Tamoxifen, in contrast, facilitated the display of mounting behavior in females when given alone or in combination with RU. Male hamsters receiving 5.0 μg of tamoxifen had high mount frequencies and slightly reduced intromission frequencies, but their ME scores were only half of control levels. Thus nafoxidine itself simultaneously promoted defeminization and antagonized masculinization while tamoxifen appeared to facilitate both processes. The data support the hypothesis that estrogens derived via aromatization from androgens play an important role in both masculinization and defeminization, at least in hamsters. The differential effects of tamoxifen and nafoxidine suggest that these and other antiestrogens might serve as useful tools for dissociating and independently examining these two components of the sexual differentiation process.     

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.     

Variation in the responsiveness of female rats to ovarian hormones as a function of preceding hormonal deprivation

Ovariectomized female rats were tested for the display of lordosis behavior 30 days after gonadectomy. They were then tested 7, 14, 21 and 81 days later following estrogen and progesterone treatment. Finally, on Day 88 of the experiment the animals were tested after either estrogen and progesterone treatment or after progesterone alone. The response to estrogen and progesterone treatment was found to be limited on the first test and on the fifth test which occurred after 2 mo without hormone treatment. When hormone treatment was repeated at seven day intervals (Tests 2–4) the tendency to show lordosis increased markedly. On the final test the animals given both hormones showed lordosis, while those which received only progesterone did not. The data suggest that the response to estrogen decreases after estrogen deprivation.     

Neonatal handling induces alteration in progesterone secretion after sexual behavior but not in angiotensin II receptor density in the medial amygdala: implications for reproductive success

Neonatal handling affects the hypothalamus-pituitary-gonadal axis in female rats. Indeed, postnatal handling induces anovulatory estrous cycles and decreases sexual receptiveness. On the other hand, Angiotensin II (Ang II) infused into the medial amygdala (MeA) reduces sexual behavior in male and female rats. Considering this, and that gonadal steroid secretion after copulatory behavior is important for reproductive success, the purpose of the present study was to investigate whether the reduction in sexual receptiveness in neonatally handled female rats is mediated by changes in Ang II receptor density in MeA. Moreover, gonadal steroid secretion after sexual behavior was analyzed. Two groups of female Wistar rats were studied: nonhandled (pups were left undisturbed) and handled (pups were handled for 1 min once a day during the first 10 days of life). Once they were 80-85 days old in the evening of the proestrus day, sexual receptiveness was recorded and after that the animals were killed by decapitation. Trunk blood samples were collected, and plasma estradiol and progesterone were measured by radioimmunoassay. The brains were removed for Ang II receptor autoradiography in MeA. The decreased lordosis quotient in the neonatally handled group was confirmed in the present study. Neonatal handling also reduced the progesterone concentration in the plasma, but did not change the estradiol and the density of Ang II receptors in MeA. The reduced progesterone could be due to the decreased lordosis frequency of handled females. However, this decreased sexual receptiveness is not mediated by changes in Ang II receptors in MeA.     

Studies on feminine sexual behavior in the male rat: Influence of olfactory stimuli

The aim of this study was to determine if the display of lordosis behavior in the male rat could be influenced by the olfactory environment. Unexperienced adult male rats were orchidectomized (ORCH). They were primed with 75 μg estradiol benzoate and 1 mg progesterone was injected at an interval of 39 hr following long-term (LT = 3 weeks) or short-term (SHT = 8 hr 30 min) exposure to the odor of male or female urine. For 10 min they were placed in the presence of a “stimulus” male of proven sexual vigor 9 hr 30 min ± 1 hr after progesterone injection. Both LT and SHT exposure to the odor of male urine caused a significant increase in the number of ORCH rats which showed lordosis response to male mounts compared to either the ORCH rats exposed to the odor of female urine or to the controls. Following complete olfactory bulb removal (COBR), no difference was observed in the occurrence of lordosis behavior between the ORCH rats whether or not exposed to the odor of urine. For the ORCH-COBR rats exposed to male urine the proportion of animals responding to mounts did not differ from that of their nonbulbectomized counterparts. In comparing the effects of COBR vs anterior olfactory bulb removal (AOBR) lordosis behavior occurred more frequently in COBR than in AOBR-ORCH rats. The lordosis quotient (LQ) was not affected by exposure to the odor of male urine in the nonbulbectomized ORCH rats. In contrast, it appeared to be higher in both COBR and AOBR animals than in their nonbulbectomized counterparts. The olfactory bulbs were then concluded to inhibit the display of lordosis behavior in the male rat. It was also thought that the olfactory stimuli originating from male urine were capable of releasing the hypothalamic structures involved in the control of lordosis behavior of the male rat from an olfactory inhibitory influence.     

Lordosis behavior in castrated male rats treated with estradiol benzoate or testosterone propionate in combination with an estrogen antagonist, MER-25, and in intact male rats

Lordosis behavior could be elicited by manual stimulation in castrated male rats after treatment with estradiol benzoate (15 μg for 10 days) or testosterone propionate (1 or 3 mg for 10 days). The effect was antagonized by treatment with the estrogen antagonist MER-25 (10mg for 10 days). Prolonged treatment with testosterone propionate (1 mg for 26 days) resulted in display of male (nine of ten rats) as well as female (seven of ten rats) sexual behavior. Eleven of 32 intact male rats (age 120 days) and 22 of 37 other intact males (age 75 days) displayed lordosis in response to manual stimulation without hormonal treatment. Seven intact males which showed lordosis without hormone treatment were injected with MER-25 (10 mg/day × 10 days) and lordosis was abolished in six cases. The results suggest that estrogen is involved in the regulation of lordosis behavior in TP-treated and intact male rats.     

Progesterone facilitation of lordosis in male and female Sprague-Dawley rats following priming with estradiol pulses

Adult male Sprague-Dawley rats rarely exhibit progesterone-facilitated lordosis following steroid treatments which are effective in females. In contrast, progesterone-facilitated lordosis has been observed following priming with estradiol pulses in another strain. The aim of this study was to compare progesterone-facilitated feminine sexual behavior in adult male and female Sprague-Dawley rats following priming with estradiol benzoate (EB) or estradiol pulses. Female sexual behavior was measured in adult, gonadectomized males and females treated as follows: Two pulses of estradiol followed by progesterone or oil the next day; EB (two doses) for 3 days, and progesterone or oil the next day. These protocols were repeated at 4- or 6-day intervals, respectively. Progesterone-facilitated lordosis was observed consistently in both sexes treated with estradiol pulses. By the fifth test, lordosis quotients did not differ between the sexes, but the lordosis ratings in progesterone-treated males remained lower than those observed in females. Proceptivity (hop-darting) was facilitated by progesterone in females, but was never observed in males. Lordosis was induced in both sexes by 15 micrograms EB, but was not reliably facilitated by progesterone. Treatment with the lower dose of EB (1.5 micrograms) induced high levels of receptivity in females (occasionally facilitated by progesterone), but not in males regardless of subsequent treatment (i.e, progesterone or oil). These data suggest that progesterone-facilitated lordosis can be induced in male Sprague-Dawley rats, if a regimen of estradiol pulses is used. Thus, the brain of the adult male is not inflexibly differentiated with regard to progesterone facilitation of feminine receptive behavior.     

Receptive behavior in developing female rats

In a series of experiments the development of sexual behavior was studied in female rats. Lordosis behavior in response to manual stimulation was induced in 100% of 19-day old females by treatment with 10 μgm estradiol benzoate (EB) and 0.5 mgm progesterone (P) and earwiggling was displayed at earlier ages. During normal development, vaginal opening preceded the display of the first receptivity in most cases, the first two behavioral sex cycles tended to be prolonged and irregular, but the subsequent cycles were of regular 4 or 5 days duration. Although treatment of immature (18-, 23- or 28-day old) females with EB (10 μgm) and P (0.5 mgm) or with EB (0.025, 0.25 or 2.5 μgm until vaginal opening occurred) resulted in precocious vaginal opening and display of sexual receptivity, the treatment did not advance the development of behavioral cyclicity. Progesterone [0.25 mgm/100 gm body weight (bw)] facilitated the display of sexual receptivity in EB-primed (0.5 or 2.5 μgm/100 gm bw) ovariectomized immature and adult female rats. Evidence was presented that behavioral sensitivity to estrogen increases with age.