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.     

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.     

Hysterectomy-induced facilitation of lordosis behavior in the rat

The present study investigated the effect of hysterectomy on hormone-induced lordosis behavior. Lordosis quotients (LQ) were measured in hysterectomized-ovariectomized (HO) and ovariectomized-sham hysterectomized (OSH) rats after several treatments including either estradiol benzoate (EB) alone or EB plus progesterone (P) 44 hr later. Testing consisted of placing the females with sexually active males 48 hr after EB. In Experiment 1, HO animals treated with 5 μg/kg EB and 0.5 mg P had significantly higher LQs than OSH animals; groups treated with 10 μg/kg plus P were not different. Experiment 2 showed that a single injection of 50 μg/kg EB resulted in equally high levels of receptivity in both groups. The LQs of HO animals injected with 3 μg/kg for 4 days did not differ from those of OSH animals; however, the administration of 0.5 mg P 24 hr after the fourth EB injection resulted in significantly higher LQs in the HO group (Experiment 3). In Experiment 4, HO rats injected with 5 μg/kg EB and 0.1 mg P 44 hr later displayed higher levels of lordosis behavior than OSH animals. It was concluded that hysterectomy facilitated the lordosis behavior of ovariectomized rats injected with both EB and P and that the mechanism for this potentiation remains to be determined.     

Independence of progesterone-induced facilitation and inhibition of lordosis behavior in ovariectomized guinea pigs

In ovariectomized Hartley guinea pigs, 15 μg progesterone was shown to facilitate lordosis in 48% of animals when administered 36 hr after a 3.3 μg injection of estradiol benzoate. This dose of progesterone also inhibited lordosis behavior in 65% of animals administered an additional 0.6 mg progesterone at 60 hr. Significant inhibition of lordosis response to the 0.6 mg progesterone existed among animals in which lordosis was not facilitated by the initial 15 μg dose of progesterone. These results show that progesterone-induced inhibition can occur without prior facilitation of lordosis as tested by the manual stimulation technique.     

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.     

Estrogen and progesterone interactions influencing sexual and social behavior in the brown lemming, Lemmus trimucronatus.

The effects of estrogen and progesterone on the social and sexual behavior of brown lemmings, Lemmus trimucronatus, were investigated. The behavior of hormone-treated and untreated ovariectomized females and sexually vigorous males was observed in six consecutive daily 5-min dyadic encounters. Sexual receptivity, as measured by lordosis, and other social behaviors including nasonasal contact, boxing postures, allogrooming, perineal investigation, and male mounting increased following 48 hr of exposure to daily injections of 0.5 μg estradiol benzoate (EB). Lordosis in EB-primed females was not facilitated or inhibited by short-term (4 hr) exposure to 0.5 mg progesterone (P). Long-term (greater than 24 hr) exposure to P apparently inhibited lordosis and other social behaviors in EB-treated females, although males continued to attempt to mount these females. In EB-treated females a dramatic increase in threat-leaps, directed by the female toward the male, was observed within 4 hr of P injection. Threat-leaps declined when P was withdrawn. Threat-leaps were also observed in ovariectomized females after prolonged exposure to P only (0.5 mg/day). Vaginal perforation and cornification were first apparent 48 hr after EB injection. P-alone treated ovariectomized females also showed vaginal perforation but cornified cells were infrequent and these animals did not show lordosis.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

Onset of the receptive and proceptive components of feminine sexual behavior in rats following the intravenous administration of progesterone

The present study was carried out in order to assess the time course of action of progesterone (P) in the facilitation of complete feminine sexual behavior. Female rats (estrogen primed via 5% E₂ Silastic capsules) were given 200 μg of P either intravenously (iv) or subcutaneously (sc), and tested for estrous behavior at $\text{1}\text{4}$, $\text{1}\text{2}$, 1, 2, and 4 hr after treatment. Among iv-treated animals, significant amounts of lordosis behavior were seen as early as $\text{1}\text{2}$ hr, and a dramatic rise in solicitation behavior was observed at 2 hr. Although sc-treated animals displayed significant amounts of lordosis and solicitation behavior at 2 hr, the behavior was not maximal until 4 hr. Intravenous administration of 400 μg P was equipotent to 200 μg P, whereas 50 μg of iv P was relatively ineffective. A dual mechanism hypothesis pertaining to progesterone's actions in the facilitation of both the receptive and preceptive components of feminine sexual behavior in rats is discussed.     

Differential sensitivity of mounting and lordosis control systems to early androgen treatment in male and female hamsters.

The effects of early testosterone propionate (TP) treatment on the adult sexual behavior of hamsters were investigated in two experiments. In Expt. I, male and female pups were injected with oil vehicle or 1, 5, 10, 50, 100, or 250 μg of TP 24 hr after birth. In Expt. II, males and females received either oil or 10 μg of TP on the day of birth (Day 1), Day 3, Day 5, Day 7, or Day 9. At 70 days of age all animals were gonadectomized and 10 days later tested for lordosis behavior after estrogen and progesterone priming. One week after the test for female behavior all females began receiving 500 μg of TP each day and were tested for mounting and intromission behavior three times at 10 day intervals. Lordosis behavior was inhibited by as little as 5 μg of TP given 24 hr after birth. In males this dose produced the maximal effect, but in females increasing dosages resulted in a proportional decrease in lordosis duration. One μg of TP neonatally facilitated later mounting and intromission behavior in females and 250 μg of TP was no more effective than 1 μg. Lordosis duration was inhibited in females by 10 μg of TP on either Day 1 or 3, however, mounts and intromissions were facilitated by TP treatment on Day 1, 3, 5 or 7. These experiments demonstrate that the mechanisms mediating masculine behavior are more sensitive to neonatal TP treatment than are the mechanisms mediating lordosis behavior.     

A possible involvement of adrenaline in the facilitation of lordosis behavior in the ovariectomized rat

In order to examine a possible role of adrenaline (AD) or noradrenaline (NA) in the control of lordosis behavior, lordosis quotient (LQ) was observed daily for 8 consecutive days in the ovariectomized rat given daily 1 or 2 microgram/0.1 ml oil of estradiol benzoate (EB) alone or together with 100 microgram/0.1 ml saline of AD or NA. AD but not NA treated together with EB caused a greater change in the daily LQ than the same dose of EB alone and the change in the daily LQ by daily treatment with both 1 microgram EB and 100 microgram AD was equivalent to that by daily treatment with 2 microgram EB alone. A half mg progesterone (P) could induce the lordosis behavior in the ovariectomized rat treated 48 hr prior with both 1 microgram EB and 50 or 100 microgram AD, but not in the one treated with 1 microgram EB alone. While 50, 100 or 200 microgram NA or 10 microgram AD had no effect, 50 or 100 microgram AD pretreated together with 2 microgram EB produced a markedly higher LQ after P than 2 microgram EB alone in the ovariectomized rat. This effect of AD on the induction of lordosis behavior was produced only when AD was pretreated simultaneously with EB and AD priming 24 or 43 hr after EB failed to elicit the effect. Therefore, it is suggested that a change of the brain target site in the estrogen sensitivity produced by AD plays a part in the control of lordosis behavior.     

The behavioral and somatic effects of ovariectomy and replacement therapy in female collared lemmings (Dicrostonyx groenlandicus)

Reproductive behavior and organ weights in intact estrous and diestrous, and in ovariectomized treated and untreated female collared lemmings (Dicrostonyx groenlandicus) were examined. Sexual behavior of intact diestrous and untreated ovariectomized females was similar, and females in both groups behaved differently from intact estrous females in scores for lordosis and mounting the male. Receptivity was observed in some females within 3 days after the first daily dose of as little as 0.1 μg of estradiol benzoate (EB) and in 83% of all females treated with 0.1 μg or more of EB for 5 days. Vaginal perforation and cornification were related to the dose of EB and length of treatment. The doses of EB used were not related to the lordosis quotient. Ovariectomy and subsequent EB treatment influenced uterine but not preputial gland weight. Adrenal weight was not influenced by ovariectomy or EB treatment, but the increased adrenal weights observed may have been related to the daily pairing of females with males.