Airway occlusion pressures in awake and anesthetized goats

The ability of intramuscular injections of gonadal steroids to exert a positive feedback action on LH secretion was investigated in the ovariectomized hen. Plasma LH was measured by radioimmunoassay. Single injections of progesterone (dose range: 0.05-10 mg/kg) or oestradiol benzoate (dose range: 0.01-1 mg/kg) did not result in an increase in plasma LH concentration. After priming with 0.1 mg oestradiol benzoate/kg on alternate days for 7 days and with 0.5 mg progesterone/kg on days 5, 6 and 7, a single injection of progesterone on day 8 (dose range: 0.1-2 mg/kg) caused the plasma LH concentration to start increasing after 15 to 30 min. Peak LH concentration was reached around 1.5-2 h after injection. The magnitude of LH response to progesterone was dose related. In contrast, a single injection of oestradiol benzoate (dose range: 0.01-1 mg/kg) failed to stimulate LH release in the oestrogen-progesterone primed ovariectomized (O-P-OVX) hen. A single injection of testosterone (dose range: 0.1-2.0 mg/kg) failed to stimulate LH release in ten out of 12 O-P-OVX hens. A small increase in LH secretion was observed in the two remaining birds. When oestrogen or progesterone was omitted from the priming schedule, a LH positive feedback response to a single injection of progesterone was not observed. Increasing or decreasing the mount of oestrogen or progesterone in the priming schedule modified the LH response to a single injection of progesterone on the day following the last priming injection. This suggested that a critical oestrogen to progesterone ratio was required to prime the LH positive feedback mechanism. It is suggested that, in the hen, the release of LH is facilitated by the positive feedback effect of a combination of oestrogen and progesterone in a two-phase process. The first is the priming phase, which depends on the presence in the blood of oestrogen and progesterone; the second is the ind .uctive phase, which depends only on an incremental change in plasma progesterone concentration. Oestrogen is not involved in the induceive phase.     

Habenular lesions and feminine sexual behavior of ovariectomized rats: Diminished responsiveness to the synergistic effects of estrogen and progesterone.

Bilateral electrolytic lesions in the habenula resulted in disruption of feminine sexual behaviors evoked by estrogen and progesterone in 43 ovariectomized rats. There were no differences between lesioned and sham-operated Ss in tests conducted after the administration of estrogen alone. Ss with lesions were characterized by an increased proportion of mounts not followed by lordosis, a decreased proportion of mounts followed by pronounced lordosis, and a decreased proportion of mounts preceded by soliciting behaviors. Lesions had a negligible effect upon the tendency to hold lordotic postures after the male dismounted. Results suggest that the habenula is involved in modulating responsiveness to the synergistic effects of estrogen and progesterone. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Mesencephalic participation in the control of sexual behavior in the female rat.

In 2 experiments with 78 female albino rats, electric stimuli applied to both pudendal nerves evoked field potentials, unit responses, and multiunit responses in the ventrolateral midbrain, in and around the peripeduncular nucleus. Bilateral lesions placed in this region suppressed sexual behavioral responses (lordosis and courting behavior) of ovariectomized Ss primed with 5, 10, 100, and 1,000 μg of estradiol benzoate and 2 mg/kg progesterone. It is proposed that the region in question represents a relay station for the integration of sensory and endocrine information concerned in the control of receptive sexual behavior in the female rat. (54 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Monoaminergic mediation of female sexual behavior.

Facilitated lordotic behavior in 18 estrogen-primed ovariectomized female Sprague-Dawley rats by direct application of progesterone or serotonergic or b-adrenergic receptor blockers to specific telencephalic, anterior hypothalamic-medial preoptic, or posterior hypothalamic sites. Blockade of the a-adrenergic system was ineffective in facilitating lordosis, as was the application of the active drugs to control sites in the thalamus or basal ganglia. Female soliciting behavior was not evoked by any of the treatments. It is concluded that the lordotic behavior component of the female rat's estrous behavior pattern is inhibited by a specific central monoaminergic system that also responds to progesterone. Soliciting behavior appears to be mediated by systems that are anatomically, and possibly neurochemically, separable from those regulating lordosis. (57 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Concurrent inhibition of sexual behavior, but not brain [–3H]estradiol uptake, by progesterone in female rats.

In 7 experiments with ovariectomized female Sprague-Dawley rats, chronic injections of high doses of progesterone (5 mg) and low doses of estradiol benzoate (EB; 2 μg) resulted in less sexual behavior than did low doses of progesterone (.5 mg) and low doses of EB. In a typical procedure for inducing sexual behavior, EB and progesterone were given sequentially, separated by 42 hrs. High levels of progesterone (2.5 and 5 mg) administered concurrently with EB inhibited the induction of sexual receptivity. Increasing the dose of EB from 2 μg to 6 μg or 10 μg offset this inhibition. High doses inhibited the induction of sexual behavior, but the inhibition waned when progesterone was administered 48 hrs prior to EB. A single injection of progesterone (1 mg) that did not inhibit the induction of sexual behavior when administered concurrently with EB did inhibit lordosis when distributed into 5 injections (.2 mg) every 4 hrs. Results of 2 experiments in which progesterone did not inhibit the uptake or retention of [–3H]estradiol by brain cell nuclei suggest that the antiestrogenic action of progesterone in the CNS is not to interfere with the binding of estradiol. (37 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sequential inhibition of sexual behavior by progesterone in female rats: Comparison with a synthetic antiestrogen.

Findings from 6 experiments show that when a large dose of progesterone was administered to ovariectomized Sprague-Dawley rats 24 hrs after a 2-μg injection of estradiol benzoate (EB), sexual receptivity was inhibited at 54 hrs (sequential inhibition). Larger doses of progesterone (1 mg) were required to inhibit the induction of sexual receptivity when tested at 54 hrs than were necessary to facilitate at 30 hrs. This inhibition was not due to copulatory stimuli from the 1st test, because inhibition occurred even when the 1st test was omitted. The inhibition was dose dependent on estradiol; increasing the EB priming dose offset the inhibition caused by 1 mg of progesterone. The results of an experiment that behaviorally dissociated the antiestrogenic action of progesterone from that of a synthetic antiestrogen, CI-628, are consistent with the notion that progesterone and synthetic antiestrogens inhibit the neural effects of estradiol by separate mechanisms of action. (32 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Lordosis behaviour in male, female and androgenized female rats

Sex differences in the lordodis response of adult rats to ovarian hormones were studied in a series of experiments. Male rats were less sensitive to oestradiol benzoate (OB, a single injection of 10, 100 or 1000 mug/kg or seven daily injections of 2, 10, or 50mglkg)then were female rats. Oestradiol benzoate-primed (10 mglkg)female, but not male, rats showed dose-dependent responses to progesterone (0-4, 2-0 or 10-0 mg/kg/. male rats responded clearly to progesterone (2 mg/rat) only when primed with a high dose of OB (100 mug/rat). Display of the whole pattern of female sexual behaviour was induced in male rats by treatment with 100 mug OB and 2 mg progesterone. Female rats treated with 1 mg testosterone propionate (TP) on day 4 of life, ovariectomized as adults and tested under the same endocrine conditions as the rats described above, retained behavioural OB sensitivity but responded poorly to progesterone. Evidence is presented that ovarian secretions during development significantly modify the response of neonatally TP-treated and normal female rats to OB in adulthood.     

Evaluation of osteocalcin and pyridinium crosslinks of bone collagen as markers of bone turnover in gingival crevicular fluid during different stages of orthodontic treatment

Treatment with serotonin reuptake inhibitors (SRIs) has been shown to cause reduced libido and anorgasmia in women. A large body of evidence suggests that serotonin may influence sexual behavior in estradiol + progesterone primed, gonadectomized female rats; however, the influence of selective SRIs on the estrous behavior of intact female rats has not been described previously. In the present study, the effect of 1 to 3 weeks of fluoxetine administration (10 mg/kg daily) on vaginal and behavioral estrus in intact female rats was studied; in addition, the effect of fluoxetine (same dose, 1-8 weeks) on copulatory behavior and on sexual motivation in hormone-primed gonadectomized rats was investigated. Subchronic administration of fluoxetine did not influence cyclicity as judged by the examination of vaginal smears but significantly reduced the percentage of rats displaying receptive behavior in the estrous phase. In addition, fluoxetine significantly reduced receptive behavior, including lordosis, in ovariectomized female rats primed with estradiol (6.25 micrograms/rat; -48 hr) plus progesterone (1.0 mg/rat, -4 hr); in contrast, sexual motivation--as reflected by the amount of time these rats elected to spend in the vicinity of a male rather than in the vicinity of a female or elsewhere--was little affected by the treatment.     

Effects of endocrine state on sociosexual behavior of female rats tested in a complex environment.

Examined the influence of both natural and artificially induced endocrine states on the sociosexual behavior of female Long-Evans rats during 15-min behavioral observations in a complex testing apparatus that allowed Ss to control their contacts with sexually active and passive males and ovariectomized (OVX) females. Ss were either intact and in various stages of the estrous cycle or OVX and treated with estradiol benzoate (5–20 μg), estradiol plus progesterone (0.5 mg/kg), or vehicle. Factor analysis of the behavioral measures indicated separate loadings on a lordotic behavior factor, a factor for Ss' preference for proximity to OVX females or passive males; and a factor for Ss' locomotion between portions of the testing apparatus. Behavioral variables loading on these factors were influenced by endocrine state, but the nature of the relation between behaviors and endocrine state varied between factors. The utility of the present testing situation in investigations of the neuroendocrine substrates underlying the motivational aspects of feminine reproductive behavior is discussed. (22 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Erratum.

Reports an error in the table of contents of the January 1975 issue, the authorship of the article "Monoaminergic Mediation of Female Sexual Behavior" beginning on page 53 should have read "Ward, Ingeborg, L., Crowley, William R., Zemlan, Frank P., and Margules, D. L." (The following abstract originally appeared in record 1975-09022-001) Facilitated lordotic behavior in 18 estrogen-primed ovariectomized female Sprague-Dawley rats by direct application of progesterone or serotonergic or b-adrenergic receptor blockers to specific telencephalic, anterior hypothalamic-medial preoptic, or posterior hypothalamic sites. Blockade of the a-adrenergic system was ineffective in facilitating lordosis, as was the application of the active drugs to control sites in the thalamus or basal ganglia. Female soliciting behavior was not evoked by any of the treatments. It is concluded that the lordotic behavior component of the female rat's estrous behavior pattern is inhibited by a specific central monoaminergic system that also responds to progesterone. Soliciting behavior appears to be mediated by systems that are anatomically, and possibly neurochemically, separable from those regulating lordosis. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Evidence that a factor besides progesterone, prolactin, or plasma-estradiol-binding protein inhibits estrogen-induced sexual receptivity in pregnant rats.

Reexamined in 4 experiments the assumption that progesterone is responsible for the inhibition of estrogen-induced receptive behavior in Wistar hooded rats. Daily administration of estradiol benzoate (EB) stimulated significantly less lordotic behavior during the 2nd half of pregnancy than in ovariectomized Ss that received sc progesterone implants, pituitary grafts that raised plasma prolactin, or both treatments combined. Following an initial facilitation of receptivity, Ss with progesterone implants showed only moderate reductions in lordosis quotients over 3 test days. The capacity of Ss' plasma to bind estradiol was found to increase significantly during the 2nd half of pregnancy. However, daily administration of a synthetic estrogen, R 2858, which is not bound by plasma protein, was no more effective than EB in stimulating receptive behavior. Administration of EB also stimulated significantly lower levels of sexual behavior in pregnant Ss than in Ss in which pseudopregnancy had been prolonged by previous hysterectomy or induction of uterine decidualization. These findings suggest that some endocrine factor other than progesterone, prolactin, or estradiol-binding protein is primarily responsible for the potent suppression of behavioral responsiveness to estrogen that occurs in pregnant rats. It is suggested that 5-alpha-reduced androgens may cause these behavioral effects. (53 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Differential effects of lesions in three limbic areas on ultrasound production and lordosis by female hamsters.

Examined ultrasound production and lordosis in 98 ovariectomized, hormone-primed (estradiol benzoate [10 μg] and progesterone [500 μg]) female golden hamsters before and after sham operations or bilateral electrolytic lesions. During 2-min exposures to synthetic ultrasounds and 1-min exposures to stimulus males, Ss with corticomedial amygdala lesions exhibited reduced ultrasound rates and lordosis durations. Following lesions in the lateral septum/bed nucleus, Ss showed significant increases in ultrasound rates but no change in lordosis. Ablations of the lateral habenula had no effect on calling but were associated with shorter lordosis durations. Results demonstrate that 2 reproductive behaviors, ultrasound production and lordosis, are differentially affected by lesion placement within the limbic system. These differences demonstrate that the neural mechanisms for 2 elements of a single major class of behavior can be distinct, both in terms of the likelihood that particular brain areas will be involved and in the nature of their involvement. (43 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Failure of protein synthesis inhibition to block progesterone desensitization of lordosis in female rats

Progesterone's desensitization effect on lordosis has been shown to correlate with a decreased concentration of hypothalamic progestin receptors after progesterone injection. In a recent study, one group of investigators found that the protein synthesis inhibitor anisomycin appeared to block progesterone's desensitization effect. Despite decreased levels of cytoplasmic progestin receptors, progesterone + anisomycin-treated rats exhibited a high level of lordosis four hr after a second progesterone injection. Because this finding conflicts with a progestin receptor model of progesterone's desensitization effect, we investigated it further. In the first experiments, ovariectomized rats were injected with estradiol benzoate followed 24 hr later by either progesterone or vehicle. Anisomycin injected 3 hr after progesterone, at a dose that causes inhibition of hypothalamic protein synthesis for at least 4 hr, was without effect on progesterone desensitization a day later. In other experiments silastic implants containing estradiol were inserted into ovariectomized rats. Forty-five hr later, rats received progesterone or vehicle, followed by injections of anisomycin or saline. Rats receiving anisomycin + progesterone were still highly receptive at 30 hr while saline + progesterone controls were not. Furthermore, the results were similar 4 hr after a second injection of progesterone at 30 hr. In a related experiment, we confirmed that anisomycin delayed dramatically termination of the period of sexual receptivity. In this laboratory anisomycin does not seem to block progesterone's desensitization effect. However, with certain procedures anisomycin delays the termination of sexual receptivity. Thus it is important in investigations of the mechanism of progesterone's desensitization effect that animals be tested prior to the second progesterone injection to determine if they are actually responding to the progesterone.     

Hypophysectomy facilitates sexual behavior in female rats

Lordosis was elecited in 49% of 87 hormonally untreated, hypophysectomized-ovariectomized (hypox-ovx) female rats in response to palpation of the flanks and perineum (vaginal stimulation was not applied). By contrast, only 12% of 113 hormonally untreated ovariectomized (ovx) rats showed lordosis in response to such stimulation. Subsequently, hypox-ovx and ovx-only rats were given daily injections of 1 mug/kg estradiol benzoate (EB) and tested for sexual receptivity with males. Teh estrogen-treated hypox-ovx females became sexually receptive significantly earlier, and exhibited higher lordosis quotients and more soliciting behavior, than the estrogen-treated ovx-only rats. The increased sexual responsiveness in the hypox-ovx rats could be due to increased LRH activity. To test this, we treated hypox-ovx rats with dihydrotestosterone propionate (DHT-P), which suppresses plasma LH levels but is relatively ineffective in inducing sexual receptivity, and found a significant depression of lordosis responsiveness. These experiments suggest that hypox-ovx females show a heightened responsiveness to hormonal and/or sensory factors that induce a lordosis response, possibly because of increased LRH activity.     

Inhibition of lordosis in rats by the antiestrogen CI-628 in the absence of progesterone.

Assessed whether the ability of the antiestrogen CI-628 to inhibit estrogen-stimulated lordosis behavior (LB) in adult ovariectomized Sprague-Dawley rats depends on its interference with the synergistic effects of estrogen with progesterone. In Exp I the effect of CI-628 was contrasted in Ss brought into estrus by estradiol benzoate (EB; 0 or 3 μg/.1 ml) combined with progesterone (P; 42 or 500 μg/.1 ml) vs 4 daily injections of EB (without P). CI-628 effectively antagonized LB in both conditions. In the absence of CI-628, Ss receiving P had significantly higher LB scores than the 4-day EB controls. In Exp II Ss receiving CI-628 on only the 1st 2 of 4 days of EB injections had decreased LB scores unless P was also given on the day of testing. This suggested that the EB from the latter injections was not acting as a progestin "mimic." In Exp III LB stimulated by EB (without P) was inhibited by CI-628 in Ss that were both ovariectomized and adrenalectomized. This suggested that adrenal progestins were not involved in the ability of CI-628 to inhibit LB. Results suggest that the mechanism of action of CI-628 for the inhibition of LB does not depend on its ability to antagonize an estrogen-induced increase in neural progestin receptors. Implications for estrogen-mediated behaviors, for which CI-628 has little or no antagonistic effects, are discussed. (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Differential effects of beta-endorphin and Met- and Leu-enkephalin on steroid hormone-induced lordosis in ovariectomized female rats

The effect of intrathirdventricular (I.T.V.) injections of beta-endorphin, anti-beta-endorphin antiserum, Met-enkephalin, Leu-enkephalin, and naloxone on the initial activation and final development of steroid hormone-mediated induction of female sexual receptivity was studied in ovariectomized female rats. The lordosis response to male mounts in ovariectomized rats after subcutaneous (S.C.) estradiol benzoate (EB) and progesterone (Prog) priming was facilitated by beta-endorphin, and Met-enkephalin (10 microg x 5 microl(-1)), but inhibited by Leu-enkephalin, when the peptides were injected into the third ventricle at the time of S.C. EB priming. A lower dose Met-enkephalin had no effects. Lordosis behavior in steroid hormone-primed rats was significantly facilitated when I.T.V. injections of Met-enkephalin were given 1 h prior to behavioral testing (47 h after EB priming). At 1 h prior to behavioral testing (47 h after EB priming), I.T.V. injection of beta-endorphin significantly inhibited lordosis behavior, especially at the higher dose of beta-endorphin (10 microg x 5 microl(-1)). Under those conditions, Leu-enkephalin had no effect. Lordosis behavior of ovariectomized female rats receiving S.C. steroid hormones and I.T.V. injection of anti-beta-endorphin antiserum was significantly inhibited when anti-beta-endorphin antiserum was injected at the time of EB priming. However, lordosis was significantly facilitated when anti-beta-endorphin antiserum was injected 1 h prior to the behavior testing (47 h after EB priming). In contrast, I.T.V. injection of the opioid antagonist naloxone given either at the time of EB priming or 1 h prior to behavioral testing (47 h after EB priming) decreased lordosis behavior. The present results suggest that 1) beta-endorphin, Met-enkephalin, and Leu-enkephalin have differential effects in the control of lordosis behavior; 2) the opioidergic systems may modulate initial-stage and final-stage estrogen-induced lordosis behavior; and 3) the opioidergic systems could be divided into the endorphinergic modulation-type and enkephalinergic modulation-type, based on their effects on lordosis behavior.     

Central progesterone induces female sexual behavior in estrogen-primed intact male rats.

Injection of progesterone induced high levels of female lordotic behavior in 10 of 47 intact, estrogen-primed male Sprague-Dawley rats when it was applied directly to the medial preoptic/anterior hypothalamic area. All 17 Ss previously had shown lordosis when the serotonergic antagonist methysergide was applied to the same central sites. Few Ss responded to systematic progesterone and none to intracranial cholesterol. Intradiencephalic Metycaine, a local anesthetic, induced lordosis in 8 Ss that previously had responded to central progesterone. These data indicate that estrogen and progesterone act synergistically to induce lordosis in male rats when progesterone is administered directly to sensitive brain sites. (37 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of repeated testing on sexual behavior of the female rat.

Investigated effects of stimulation during repeated testing, using 24 female Sprague-Dawley rats in which intromission was prevented by a vaginal mask. Ss were ovariectomized and administered 1 mg of estradiol benzoate (EB) daily for 10 days (Exp I) or 5 mg of EB for 2 days (Exp II). Behavioral indices included lordosis quotient (a measure of sexual receptivity) and rejection quotient (a measure of social rejection of the male). Intensity and duration of lordosis gave additional measures. In Exp I hourly testing increased lordosis quotient and duration, especially in Ss receiving EB for 5 days; no effects of daily testing were shown. Exp II compared the behavior of Ss that were either handled hourly and tested hourly with the male rat or only handled hourly to the behavior of Ss that were tested and handled only once. Repeated testing and/or handling facilitated sexual responsiveness, while Ss that received neither treatment were sluggish in their social response to the male rat when they were tested, and were not sexually receptive. (17 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The effects of aging on mu and delta opioid receptors in the spinal cord of Fischer-344 rats

The lordosis-inhibiting effects of the 5-HT1A receptor agonist, (+/-)8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), were examined in ovariectomized rats, hormone primed with 2.5, 7.5, or 25 micrograms estradiol benzoate plus 500 micrograms progesterone. 8-OH-DPAT (50, 100 or 200 ng per bilateral site) infused into the ventromedial nucleus of the hypothalamus (VMN), inhibited lordosis behavior in all hormone-treated conditions. However, animals primed with 2.5 micrograms estradiol benzoate were significantly more affected by the infusion than rats primed with 7.5 or 25 micrograms of the hormone. These findings strengthen prior speculations that 5-HT1A receptor function is modulated by estrogen.     

Estrogen improves performance of reinforced T-maze alternation and prevents the amnestic effects of scopolamine administered systemically or intrahippocampally

In a previous study, administration of high doses of estradiol benzoate (100 microgram/kg for 3 days im) to ovariectomized Long-Evans rats counteracted impairments of reinforced T-maze alternation induced by systemic administration of scopolamine, a muscarinic receptor blocker. In the current study, daily administration of lower doses of estradiol benzoate (5 microgram/kg for 3 weeks sc) increased the number of correct reinforced alternations during T-maze acquisition in ovariectomized rats compared to oil-treated controls and prevented impairments of reinforced alternation induced by injection of scopolamine hydrobromide (0.2 mg/kg ip). Furthermore, scopolamine (20 microgram) delivered bilaterally to the dorsal hippocampus reduced reinforced T-maze alternation in ovariectomized rats previously trained to complete this task while daily treatment with estradiol benzoate (5 microgram/kg sc) for 1 week prior to scopolamine infusion counteracted this impairment. In summary, physiological levels of estrogen improved performance during acquisition of reinforced T-maze alternation and prevented impairments induced by scopolamine administered systemically or intrahippocampally.