Hormonal Modulation of the Cutaneous Initiation of Lordosis in Infant and Adult Rats

The purpose of these experiments is to compare the regional specificity (Experiment 1) and the hormonal modulation (Experiment 2) of the cutaneous initiation of lordosis in 4- to 6-day-old male and female rats (infants) and in 60- to 90-day-old female rats (adults). In Experiment 1, subjects were primed with 100 μg estradiol benzoate (EB) and 0.5 mg progesterone (P) and were denervated on the Waist (dermatomes L1-L3), Midriff (dermatomes T10-L3), Flanks (dermatomes L4-L6), or Sides (dermatomes T10-L6). In infants, there were no significant differences between males and females. Denervation of the Waist. Midriff, or Sides but not of the Flanks significantly decreased the percentage of subjects displaying lordosis, lordosis quotient (LQ), and mean lordosis duration; no significant differences were obtained among Waist-, Midriff-, or Sides-denervated infants. In contrast, denervation of the Sides but not of the Waist significantly decreased LQ and mean lordosis intensity among adults. In Experiment 2, Waist-denervated infants and their surgical Controls were treated either with 100 μg EB and 0.5 mg P or with the oil vehicle; Waist-denervated adults and their surgical Controls received either 100 or 10 μg EB (no P). Regardless of hormone treatment, denervation of the Waist significantly decreased LQ and lordosis duration in infants and decreased LQ and lordosis intensity in adults. In infants, the only effect of priming with EB and P was to increase the percentage of pups showing lordosis and lordosis duration among the surgical Controls. In contrast, priming with 100 μg EB significantly increased the percentage of rats displaying lordosis, LQ, and lordosis intensity among Waist-denervated adults. These data suggest that cutaneous input from the Waist is important for eliciting lordosis in both infant and adult rats, and that the importance of this input is modulated by hormone priming in adult but not infant rats.     

Inhibition of estrogen facilitation of sexual behavior by the intracerebral infusion of actinomycin-D

It has been shown previously that intracerebral actinomycin-D (Act-D) pellets inhibit estrogen facilitated female sexual behavior, but it was not possible to test the reversibility of this effect. In the present study an attempt was made to distinguish between the possible temporary interruption by Act-D of the biochemical action of estrogen which facilitates sexual receptivity and permanent toxic effects of the drug. Act-D in saline was infused into the third ventricle or the preoptic area (POA) to determine whether a reversible suppression of sexual behavior as measured by the lordosis quotient (LQ) could be produced. Ovariectomized rats were implanted with midline guide tubes entering the third ventricle (eight rats) or with bilateral tubes extending to the corpus callosum above the POA (67 rats). Each animal served as its own control since pretest and Act-D and recovery tests were performed 10–14 days apart in most subjects. For each behavioral test implanted subjects were primed with 3μg estradiol benzoate (EB) and 0.5 mg progesterone (P) 48 hr later. Behavioral tests, each involving 50 mounts, were performed 4–6 hr after P. Following the pretest the animals were retested under experimental conditions. Inner cannulae were inserted into the POA through the guide tubes and 0.11 μg Act-D infused 24 or 12 hr before, simultaneously with, or 6, 12, 18, or 26 hr after EB. A recovery test was performed 10–14 days later with no intracerebral infusion. The control procedure (infusion of of saline either simultaneously with or 12 hr after EB) did not alter the LQ. Act-D infusion produced a reversible suppression of lordosis which was dependent upon the time of administration of Act-D. Intraventricular infusion of Act-D 6 hr after EB reversibly inhibited lordosis behavior and no lesions were produced. Act-D infused into the POA simultaneously with EB or 6 hr later reversibly suppressed the LQ. In the 6 hr group, for example, the LQ fell from 78.3 to 35.7, but 10–14 days later reached 74.3. Although brain lesions of varying extent were produced by Act-D, the marked but reversible suppression of lordosis behavior is consistent with the view that Act-D inhibits estrogen facilitation of lordosis behavior by means of a biochemical rather than cytotoxic action.     

Duration of estrogen stimulation and progesterone inhibition of maternal behavior in pregnancy-terminated rats

The duration of the effectiveness of estradiol benzoate (EB) on the latency to the onset of maternal behavior was measured in 16-day pregnant rats that were hysterectomized-ovariectomized (HO). Eight groups of HO animals were treated with either a single SC injection of 5 μg/kg of EB or oil at surgery and were initially presented with foster pups at either 24, 48, 72, or 96 hr postoperatively. Compared to their respective controls, EB-treated animals showed singificantly shorter latencies when testing began at 48 and 72 hr but not 24 or 96 hr. In the second experiment, 16-day HO rats were treated with 5 μg/kg of EB at surgery and either oil or 0.5 mg of progesterone at 0, 24, or 44 hr postoperatively. Additional groups received either progesterone or oil at surgery (instead of EB) and a second injection of oil 44 hr later. Testing began 48 hr following surgery for all groups, and the results showed that only the groups injected with EB alone or EB plus progesterone at 44 hr displayed short-latency maternal behavior. It was concluded that a significant reduction in the latency to the onset of maternal behavior can be obtained between 24 and 72 hr after EB treatment and that progesterone when injected concurrently or 24 hr later can inhibit the effectiveness of EB.     

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.     

Effects of the antiestrogens,MER-25 and CI 628, on rat and hamster lordosis

Antiestrogens were used to test the hypothesis that estrogen exerts a “maintenance,” as well as a “priming,” effect on rat and hamster sexual receptivity as it apparently does for guinea pigs. MER-25 (75 or 150 mg/kg) significantly reduced rat LQ when given ?2 hr or 8 hr after EB injection. MER-25 given at 34 hr (2 hr prior to P) failed to diminish rat LQ. With hamsters, MER-25 in large doses (750 mg/kg) given either at ?2 hr or 34 hr reduced lordosis duration to 40% of controls, but this effect was confounded by severe illness among the MER-25 injected animals. Lower doses failed to block behavior, but still produced some toxicity. CI 628 (50 mg/kg) greatly reduced hamster lordosis duration and increased lordosis latency when given 0 hr, but not 34 hr, after EB. The results are consistent with similar previous work on rats and do not support the concept of estrogen “maintenance” in either rats or hamsters.     

Hormonal basis of hysterectomy-induced maternal behavior during pregnancy in the rat.

Hysterectomy during the last half of pregnancy (i.e., Day 10–19) induces a rapid onset of maternal behavior; ovariectomy in addition to hysterectomy, prevents this effect. Estradiol and progesterone were tested for their ability to restore short-latency maternal behavior in hysterectomized-ovariectomized (HO) females operated on the 10th, 13th, 16th and 19th days of pregnancy. A single injection of either 20 μg/kg or 100 μg/kg estradiol benzoate (EB) immediately following HO either alone or followed by 0.5 mg progesterone (P) 44 hr later restored short-latency maternal behavior similar to that observed following hysterectomy only. The lower dose of EB was found to be equally effective at all stages of pregnancy and P was unnecessary to induce maternal behavior. The effectiveness of EB in inducing maternal behavior was discussed in relation to the hormonal changes which follow hysterectomy during pregnancy and to those which are associated with the normal onset of maternal behavior around parturition.     

Facilitatory and Inhibitory Effects of β-Endorphin on Lordosis in Female Rats: Relation to Time of Administration

The purpose of the present study was to investigate the effect of time of β-endorphin (β-EP) administration on lordosis in ovariectomized female rats injected subcutaneously (sc) with estradiol benzoate (EB) and progesterone (Prog). Intracerebroventricular (icv) injections of β-EP and naloxone (NLX), an opioid receptor antagonist, were administered at the various stages of sc steroid hormone priming. Facilitation of lordosis induced by 10 μg β-EP was observed exclusively within the initial 6 h of estrogen action, after which inhibition of lordosis occurred. At 12 h after EB priming, at the time of sc Prog treatment (or 43 h after EB priming), icv injection of 10 μg β-EP significantly inhibited lordosis. Lordosis was significantly facilitated by icv injections of 1 and 10 μg β-EP at the time of sc EB priming, but not by 0.1 μg β-EP. A dose–response relationship was identified for lordosis in experimental animals receiving icv injection of β-EP. Lordosis was inhibited by icv injections of 1 and 10 μg β-EP at 1 h before the test (or 47 h after EB priming). Lordosis was significantly inhibited by icv injection of NLX at all stages. From the present results, it seems that two different mechanisms are involved in endorphinergic modulation of rats' sexual receptivity: (a) the endorphinergic system at the initial stages of estrogen action facilitates the estrogen activation of lordosis; (b) the endorphinergic system at the final stages of steroid action inhibits lordosis. Moreover, there exists a critical time between 6 and 12 h after estrogen priming for endorphinergic mediation to modulate estrogen action.     

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.     

The role of the uterus in regulation of heat duration in cycling rats

These experiments examined the effects of hysterectomy on heat duration and on the reinduction of estrous behavior by progesterone (P) following the termination of spontaneous heat in 4-day cycling rats. Hysterectomy did not affect the onset of estrus but prolonged heat duration. The average duration of sexual receptivity for hysterectomized (H) and sham-hysterectomized (SH) rats was 18.2 and 13.0 hr, respectively. Furthermore, H animals injected with either 0.5 mg P within 2 hr, or 4.0 mg P 24 hr following the termination of natural estrus showed significantly higher lordosis and solicitation responses than SH rats similarly treated. These behavioral findings were correlated with the level of hypothalamic progestin receptors. That is, H animals had a significantly higher concentration of progestin receptors than SH rats immediately following the termination of spontaneous heat and also 24 hr later. Both in estrous-cycling rats and in gonadectomized animals treated with estradiol benzoate (EB), hysterectomy resulted in higher serum estradiol (E2) levels. The results of these experiments suggest that prolongation of the period of sexual receptivity and the facilitated behavioral responses to P following the cessation of estrus in hysterectomized animals may be due to a lowered clearance rate of circulating estradiol which presumably enhances the estrogen conditioning of the neural substrates.     

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.     

Suppression of lordosis in guinea pigs by ethamoxy-triphetol (MER-25) given at long intervals (34-46 hr) after estradiol benzoate treatment

Ovariectomized guinea pigs were given estradiol benzoate (EB) followed 40 hr later by progesterone (P). Behavioral testing commenced 1 hr after P injection and continued at hourly intervals for 8 hr. This treatment activated lordosis in almost 100% of animals. Administration of the antiestrogen MER-25 (75 mg/kg body wt per injection) between 2 hr before and 6 hr after EB treatment did not cause a significant decline in proportion of animals displaying lordosis, but did cause a decrease in length of time the lordosis position was held (maximum lordosis, sec). In contrast, $\text{13}\text{14}$ animals given MER-25 at 2 hr before and 2 hr after P and $\text{8}\text{10}$ animals given MER-25 simultaneously with and 2 hr after P, failed to show lordosis. Administration of supplementary EB at around the time of P injection, partially alleviated these behavior-blocking effects of MER-25. When MER-25 was given 2–6 hr after administration of P there was a significant decrease in duration of heat (hr). These results suggest that in addition to its early “triggering” effects, estrogen has important “maintenance” effects which determine the character of heat in guinea pigs. Continued presence of estrogen in the nervous system may be a requirement for the facilitatory actions of P on sexual behavior in guinea pigs, but such a requirement may not exist in other rodents such as rats.     

Masculinization and defeminization induced in female hamsters by neonatal treatment with estradiol, RU-2858, and nafoxidine

Newborn female hamsters were treated with 0.1 or 1.0 ng of estradiol benzoate (EB), with 1.0 ng–2.0 μg of the synthetic estrogen RU-2858, or with 0.1 or 0.5 μg of the antiestrogen nafoxidine. When adult the animals were treated with EB and progesterone and tested for the display of lordosis and with testosterone propionate and tested for the display of mounting behavior. The EB doses used failed to alter sexual differentiation. RU-2858 masculinized and defeminized in a dose-dependent manner being most effective when given neonatally as two divided doses. Nafoxidine inhibited lordosis without enhancing mounting behavior. The findings support the hypothesis that estrogens may be involved in the normal sexual differentiation process.     

Aromatization and the induction of male sexual behavior in male, female, and androgenized female hamsters

Eight weeks after gonadectomy male, female, and androgenized [10 μg testosterone propionate (TP), 24 hr after birth] female hamsters were given daily treatment with: 150 μg dihydrotestosterone (DHT), 5 μg estradiol benzoate (EB), 150 μg DHT + 5 μg EB, 150 μg DHT + 1 μg EB, 30 μg DHT + 5 μg EB, 30 μg DHT + 1 μg EB, or the oil vehicle. Treatment of castrated male hamsters with 5 μg EB fully restored mounting but relatively few of these animals intromitted and none ejaculated. Treatment with 150 μg DHT restored all components of male sexual behavior but only in a small proportion of the males. Combined treatment with EB and DHT restored mounts, intromissions, and ejaculations in the majority of the males. Although as little as 30 μg DHT + 1 μg EB restored the full complement of male behavior, the males which received 150 μg DHT + 5 μg EB or 150 μg DHT + 1 μg EB required fewer intromissions to achieve ejaculation than the males which received 30 μg DHT + either dose of EB. The response of the androgenized females was similar to that of the males except that the androgenized females had lower intromission rates and none ejaculated. Relatively few of the nonandrogenized females responded to EB and DHT treatment and those that did mounted only a few times each test. These results demonstrate that both EB and DHT can stimulate male sexual behavior in the hamster and that the sensitivity to EB and DHT for copulatory behavior is determined by early postnatal androgen exposure.     

RU486 facilitates or disrupts the sensitization of sexual behaviors by estradiol in the ovariectomized Long–Evans rat: Effect of timecourse

An acute injection of estradiol benzoate (EB) to the ovariectomized (OVX) rat activates low levels of lordosis, and subsequent progesterone (P) administration augments lordosis and recruits a complete pattern of sexual behavior including appetitive behaviors (e.g., hops/darts and solicitations). However, repeated injections of 5 μg or 10 μg EB (but not 2 μg EB), administered every 4 days to sexually-experienced OVX rats results in a behavioral sensitization, such that lordosis quotients (LQs) and appetitive behaviors progressively increase. We have shown that adrenal P does not play a critical role because behavioral sensitization to EB is not prevented by adrenalectomy. Here we tested whether P receptors play a role by examining the effect of chronic administration of the P receptor antagonist RU486 at a dose that reliably inhibits sexual behavior in fully primed OVX rats. Females were treated with EB (5 or 10 μg), and 5 mg RU486 dissolved in 0.4 mL vehicle (VEH; 80% sesame oil, 15% benzyl benzoate, 5% benzyl alcohol) 48 h and 5 h prior to each of 7 tests, respectively, occurring at 4-day intervals in unilevel 4-hole pacing chambers. Control animals were treated with 2, 5, or 10 μg EB + VEH. As expected, sensitization did not occur in females treated with 2 μg EB + VEH, and those females received fewer intromissions and ejaculations than all other groups. RU486 did not prevent the sensitization of LQ, moderate and high lordosis magnitudes (LM2 and LM3) or appetitive sexual behaviors on early tests, and in fact potentiated appetitive behaviors, LQ, LM2 and LM3, consistent with its facilitative actions in females treated with EB-alone, as we and others have reported previously. However, despite the initial facilitation, blocking P receptors by chronic administration of RU486 inhibited the maintenance of behavioral sensitization to EB.     

Inhibitory actions of progesterone on hormonal induction of estrus in female guinea pigs.

Biphasic actions of progesterone (P) were studied in three groups of guinea pigs injected with 3 μg estradiol benzoate (EB) followed 36 hr later with either .05, 0.4, or 5.0 mg P. All animals in each group displayed estrous behavior within 5–7 hr after P. Groups differed, however, in their response to a second sequence of 3 μg EB and 0.4 mg P initiated 9 hr after the first or prior P. Percentages of females displaying estrous responses were 100, 50, and 0 in the .05, 0.4, and 5.0 mg groups, respectively.Radioimmunoassay of P at varying times after the first or prior injection showed that concentrations in the plasma declined to baseline within 9–18 hr for animals given prior injections of .05 mg P, within 36 hr for those given 0.4 mg P, and remained elevated throughout for 45 or more hr for those given 5.0 mg P.A second experiment showed that the inhibitory effect of 1.0 mg P given to spayed females without prior estrogenization (direct inhibition) was inversely related to the time elapsing between that injection and the initiation of a sequential regimen consisting of 6 μg EB and 0.4 mg P, and also demonstrated that 0.05, 0.1, 0.25, 0.5, or 1.0 mg P given 2 hr before the sequential regimen results in a dose-related inhibition. Thus, prior facilitation of lordosis is in no way essential for inhibition with exogenous P, and variables that regulate degree of biphasic inhibition also regulate direct inhibition.     

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.     

The inhibition of steroid-induced sexual behavior by intrahypothalamic actinomycin-D

Lordosis behavior can be elicited in the ovariectomized rat after treatment with estradiol benzoate (EB) and progesterone (P) injections, but the EB must act for an extended period before P can facilitate this behavior. The possibility that this action of EB involves the stimulation of RNA or protein synthesis was tested by implanting actinomycin D (Act-D) directly into the preoptic area, one probable site of estrogen action. A total dose of 0.18 μg Act-D in bilateral cocoa butter pellets significantly inhibited lordosis behavior when implanted 12 hr after the injection of 3 μg. but not 15 μg EB. Implantation of this dose of Act-D subcutaneously, or intrahypothalamically 32 hr after EB injection, was without effect. Act-D placed in the ventromedial hypothalamus also suppressed lordosis, but implants in the caudate nucleus were without effect. At the time of the behavioral tests the animals were in excellent condition as determined by calculation of a health score, and no physical lesions were evident at the site of the implants. However, it was impossible to test the reversibility of this suppression of lordosis behavior since the animals became ill and many died within 1–2 weeks of implantation. The present results are consistent with, but not proof of, the concept that RNA synthesis may be essential for steroidinduced sexual behavior.     

Endogenous progesterone and lordosis behavior in male rats given estrogen alone

Male rats castrated as adults were given successive doses of estradiol benzoate (EB) combined or not, with dexamethasone (DEXA) at the end of estrogen treatment. Two experiments were done to determine if progesterone (P) of adrenocortical origin was involved in the display of lordosis behavior under these experimental circumstances. There was a significant rise in blood P concentration in animals given 0.5 and 1.0 microgram EB when compared with oil-control injected animals, an effect which was completely suppressed by DEXA treatment. An increase in the proportion of estrogen treated animals displaying lordosis responses to male mounts was found with increasing doses of EB and paralleled the effects of EB on P adrenocortical secretion. However, the number of feminized animals given 1 microgram EB + DEXA was reduced to the level corresponding to the effects of 0.5 microgram EB on lordosis behavior. These data show that the secretion of P by the adrenals is involved in the expression of lordosis behavior in castrated male rats primed with repeated doses of estrogen.     

The comparative potency of various steroids to complete the priming process for lordosis in guinea pigs

Ovariectomized adult guinea pigs were treated with a regimen of estradiol benzoate (0.2 μg/animal estradiol benzoate at hr 0 and 19) that was shown to be minimally effective for the induction of lordosis. They were then treated with 10, 20, or 80 mg of enclomiphene, 5, 20, 40, or 100 μg of estradiol, or testosterone, cortisol, estrone, estriol, diethylstilbestrol, catechol estradiol, or catechol estrone (all at a dose equivalent to 5 μg of estradiol) at hr 28. At hr 39 all females were given 0.5 mg progesterone, and subsequently tested for lordosis behavior. Of the various agents injected at hr 28 only estradiol (at all doses given), estrone, estriol, and diethylstilbestrol were effective in supporting display of lordosis behavior. The results indicate that the antiestrogen enclomiphene, the catechol estrogens, and at least some C₁₉ and C₂₁ steroids are weaker than E₂ or ineffective in facilitating lordosis behavior when given late in the priming period. Because previous work had shown that enclomiphene has partial estrogenic effects on lordosis behavior when administered early in the priming period (i.e., at hr 0, 19), it is suggested the early and late phases of the priming process induced by E₂ entail qualitatively different neural processes.     

Induction of lordosis responsiveness by vaginal stimulation in rats is independent of anterior or posterior pituitary hormones

In a previous study, rats that initially did not show lordosis in response to palpation of the flanks and perineum started to show lordosis to this stimulus when tested 10 sec after brief vaginal stimulation and continued to show lordosis responsiveness for more than 3 hr. In the present study, we tested the possibility that this effect of vaginal stimulation is mediated by the release of pituitary hormones. Hypophysectomized rats showed the lordosis-activating effect of vaginal stimulation, and this effect persisted for more than 1 hr, similar to rats with intact pituitaries. Oxytocin (50 or 100 mU/rat) or vasopressin (100 mU/rat) injected systemically did not induce lordosis responding in ovariectomized rats that received either a single injection of estradiol benzoate (2 μg/Kg) or no hormonal treatment. However, these individuals subsequently showed the lordosis-activating effect of vaginal stimulation. The mechanism by which vaginal stimulation activates lordosis responsiveness thus appears to be due to some process other than release of pituitary hormones.