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PubMed1986

Preoptic lesions increase the display of lordosis by male rats.

Male rats do not normally show feminine patterns of sexual behavior even when injected with the ovarian hormones estrogen and progesterone. We find that brain lesions which damage the preoptic-anterior hypothalamic continuum augment the display of lordosis in hormone-treated male rats. The most effectively feminizing brain lesions are ones which bilaterally destroy a substantial portion of the medial preoptic area encompassing the sexually dimorphic nucleus of the preoptic area (SDN-POA). Males with particularly large preoptic lesions are receptive following estrogen treatment and show a progesterone facilitation of receptivity. In this respect, they cannot be behaviorally distinguished from females. Thus, axons originating in and/or passing through the preoptic area apparently inhibit the display of feminine sexual behaviors in males. Preoptic development and lordosis are each predictably affected by perinatal stimulation by testicular hormones, and hormone-stimulated preoptic development may form the neurological basis for some of the defeminizing effects of perinatal hormonal exposure. Our results raise the possibility that the site of this behavioral defeminization is the SDN-POA.

Animals↗
PubMed1987

Effects of hypothalamic serotonin depletion on lordosis behavior and gonadal hormone receptors.

The effects of chronic depletion of serotonin on feminine sexual behavior (lordosis), cytosolic progestin receptors and estradiol nuclear receptors were investigated. Intrahypothalamic administration of 5,7-dihydroxytryptamine (5,7-DHT) markedly enhanced lordotic responding in estradiol benzoate (EB)-primed, 5,7-DHT-treated female rats and in EB-progesterone primed, 5,7-DHT-treated male rats. Cytosolic progestin receptors were measured in preoptic-hypothalamic nuclei related to reproductive function in sham and 5,7-DHT-treated rats after EB priming. In both sexes, no differences between sham and 5,7-DHT-treated subjects were noted for progestin binding in the medial preoptic nucleus, ventromedial nucleus or arcuate-median eminence area. Estrogen-nuclear complexes were measured in the same brain nuclei of female rats following EB priming, and no differences between sham and 5,7-DHT-treated rats were found. Under the conditions employed, it would appear that, despite marked elevations in lordotic responsivity, the accumulation of estrogen nuclear receptors and the levels of estrogen inducible progestin receptors remain unaltered after chronic depletion of serotonin. Thus, serotonergic influences on lordosis do not appear to involve changes in the expression of steroid receptor levels in preoptic-hypothalamic nuclei known to mediate hormone-dependent neuroendocrine processes.

5,7-Dihydroxytryptamine↗
PubMed1991

GABAergic-serotonergic interactions in regulating lordosis.

The GABAB agonist, baclofen, causes a dose-dependent decrease in lordosis, and this effect is attenuated following hypothalamic serotonin, (5-HT) lesions. Baclofen administration is associated with decreased 5-HT activity in the medial preoptic (mPOA) and ventromedial nuclei and enhanced 5-HT activity in the midbrain central gray, and with enhanced norepinephrine activity in the mPOA. Interactions between gamma-aminobutyric acid (GABA) and 5-HT may, therefore, be important for the activation of lordosis.

5,7-Dihydroxytryptamine↗
PubMed1994

Agonist activation of 5-HT1A receptors in the median raphe nucleus and female rat lordosis behavior.

Proestrous rats were infused unilaterally into the median raphe nucleus with 200-2,000 ng of the 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). Inhibition of the lordosis to mount ratio occurred within 15 and 10 min, respectively, following infusion with 1,000 or 2,000 ng of the drug. Infusion of 2,000 ng of the 5-HT2 agonist, (+/-)-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI), or 4,000 ng 5-HT (creatinine sulfate) failed to substantially reduce lordosis behavior.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

The effects of long-term treatment with 8-OH-DPAT on the lordosis response and hypothermia in female rats.

The effects of long-term treatment with a low dose of the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) on steroid hormone-dependent copulatory behaviour in female rats, the lordosis response, and on the hypothermic response of female rats were studied. Female rats were treated for 15 days, once daily, and tested on days 1 and 15 of treatment. They received 25 micrograms/kg on test days and 50 micrograms/kg on all other days. Subsensitivity was not induced to the inhibitory effect of 8-OH-DPAT on the lordosis response. In contrast, however, the acute effect of 8-OH-DPAT on body temperature was abolished by the long-term treatment. The results presented indicate that the induction of subsensitivity to the effects of 8-OH-DPAT is not primarily dependent on the pre- or post synaptic locus of action. Our data suggest that hormonal mechanisms are involved.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1983

Long-term (39--51 hr) exposure to estradiol in silastic capsules and lordosis behavior of guinea pigs.

Three dosage levels of estradiol (E2) in Silastic capsules were administered to ovariectomized guinea pigs for periods of 39 or 51 hr. At 39 hr., a systemic injection of progesterone was given, and hourly testing began. Dose-dependency of various aspects of lordosis behavior was established at both time intervals, and the serum E2 levels produced by the medium and high dosage levels bracketed those found at the proestrus peak in intact guinea pigs. Although there were no significant behavioral differences between the 39- and 51-hr groups at the individual dosage levels, when the data from all three dosage groups were collapsed, exposure for 51 rather than 39 hr was seen to produce increases in maximum lordosis and heat-duration measures. The results suggest that subtle facilitative effects of estrogen occur very late in the estrogen-conditioning process (even after progesterone is administered).

Animals↗
PubMed1990

Chemical structure of corticosteroids and its relationship with their acute induction of lordosis in the female rat.

The intravenous injection of several corticosteroids in the spayed estrogen-primed rat resulted, 5 min later, in a remarkable induction of lordosis response for deoxycorticosterone and 11-deoxycortisol. A lower but important effect was induced with corticosterone and 17 alpha-hydroxyprogesterone. A chemical structure-biological effect analysis showed that C-21 hydroxylation (e.g., deoxycorticosterone, 11-deoxycortisol, and corticosterone) induces the behavioral effect. However, C-11 or C-17 hydroxylation alone promotes the lordosis response to a lesser degree (corticosterone and 17 alpha-hydroxyprogesterone, respectively). However, the effect of these latter compounds is significant. From the results, it is concluded that deoxycorticosterone and 11-deoxycortisol along with other steroids such as 20 alpha-hydroxyprogesterone are suitable candidates for synergizing the well-known estrogen-progesterone induction of lordotic behavior.

Adrenal Cortex Hormones↗
PubMed1984

Beta-endorphin suppression of lordosis behavior in female rats; lack of effect of peripherally-administered naloxone.

Endogenous opioid peptides have been implicated in the control of copulatory behavior of the male rat. In order to assess the possible role of opioids in modulation of sexual receptivity in the female rat, lordosis behavior of ovariectomized (OVX) steroid-primed rats was tested after administration of beta-endorphin (B-END) or naloxone (NAL). Lordosis-to-mount ratio (L/M) of estrogen (E) - and progesterone (P) -primed rats was suppressed 15 and 45 minutes after intraventricular infusion of 100 ng B-END. This suppressive effect was blocked by subcutaneous injections of NAL (2 mg/kg). NAL alone, however, failed to enhance L/M in E-primed rats when administered in subcutaneous doses of 2 or 40 mg/kg. Thus, B-END is capable of suppressing lordotic responsiveness, but endogenous B-END does not appear to tonically suppress responsiveness in the E-primed rat.

Animals↗
PubMed1996

Protective actions of the 5-HT2A/2C receptor agonist, DOI, on 5-HT1A receptor-mediated inhibition of lordosis behavior.

Sexually receptive proestrous rats were infused bilaterally into the ventromedial nucleus of the hypothalamus (VMN) with 200 ng of 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), 1000 or 2000 ng of 5-methoxy-3-(di-n-propylamino) chroman (5-MEO-DPAC), or 1000 or 2000 ng of serotonin (5-HT) plus or minus the 5-HT2A/2C agonist, (2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI). DOI protected against the lordosis-inhibiting effects of 5-HT and each of the 5-HT1A agonists. These results substantiate a prior report that 2000 ng DOI could protect against the lordosis-inhibiting action of 200 ng 8-OH-DPAT and demonstrate that such protection is not unique to a single 5-HT1A agonist. Consequently, these results strengthen evidence that functionally significant interactions occur among 5-HT receptors within the VMN.

Amphetamines↗
PubMed1975

Neonatal hormone experience and adult lordosis and fighting in the golden hamster.

Androgenization by testicular secretions or exogenous testosterone propionate (TP treatments administered 24-48 hr post partum) suppressed sexual receptivity in the golden hamster. In response to prolonged adult estradiol benzoate (EB) treatment, gonadectomized normal females and neonatally castrated males exhibited significantly longer total lordosis durations than normal male or neonatally TP-treated (20 mug or 200 mug) females. These results suggest that one aspect of androgen-induced masculinization in the hamster involves reduced estrogen sensitivity. Responses to sequential EB followed by progesterone treatment were also lower in the androgenized groups. Neonatally castrated males did not differ significantly from normal females in their lordosis behavior. Irrespective of adult hormone treatment, androgenized animals fought more than normal females or neonatally castrated males. A genital mask was used to reduce sex differences in peripheral stimulation during testing.

Age Factors↗
PubMed1977

Effects of acute ovariectomy on the lordosis response of female rats.

The sexual receptivity of intact females with 4- or 5-day estrous cycles was compared to that of other females which had been ovariectomized at particular times during their cycles. The quality and frequency of lordosis responding were more degraded the earlier during the cycle ovariectomy was performed. This effect was more pronounced in 4-day than in 5-day cyclic females. Because exogenous progesterone was administered to all ovariectomized females, these behavioral deficits were attributed to removal of ovarian estradiol. Ovariectomy 6 hr before the critical period for luteinizing hormone release significantly shortened the duration of behavioral estrus, even though it had no effect when lordosis was tested at the time intact estrous females are maximally receptive. These findings are consistent with the hypothesis that the continual availability of estradiol throughout the 18--24 hr interval perior to the onset of behavioral estrus is essential for optimal conditioning of sexual receptivity to occur under physiological conditions. The relevance of triggering and maintenance functions of estradiol to these results is discussed.

Animals↗
PubMed1982

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.

Animals↗
PubMed1985

Food intake, body weight and lordosis in male and female mongolian gerbils: effects of ovarian steroids.

The effects of gonadectomy and ovarian hormone treatment on food intake, body weight, and lordosis in male and female Mongolian gerbils were examined. In female gerbils, a significant decrease in food intake and body weight was observed after ovariectomy, with estradiol benzoate (1, 10, or 100 micrograms/day) increasing food intake in a dose dependent fashion. However, the dose of estrogen (1 microgram) that restored food intake and body weight to control levels in ovariectomized animals was lower than that required to elicit maximal sexual receptivity. Progesterone, when given in conjunction with estrogen, significantly facilitated the effect of estrogen on food intake without further altering body weight. In male gerbils, castration produced a significant but transient increase in body weight and a delayed increase in food intake. Unlike female gerbils, male gerbils exhibited no significant alterations in food intake, body weight, or lordosis in response to treatment with ovarian steroids. The present results are compared to those obtained in other species.

Animals↗
PubMed1986

Facilitation of lordosis by estradiol in the mesencephalic central gray.

Ovariectomized female hamsters received unilateral implants of estradiol aimed at the mesencephalic central gray (MCG). Postoperative levels of lordosis and ultrasonic vocalization were used to evaluate implant effects on sexual receptivity and proceptivity. Females with large MCG implants showed higher levels of receptivity than females with similar implants at control sites. In addition, females with small MCG implants showed little receptivity while the implant served as the sole source of estrogen, but diverged from controls by showing elevated receptivity during supplemental treatment with low systemic doses of estradiol. These results suggest that estradiol implants in the MCG facilitate receptivity if, and only if, accompanied by exposure of other brain areas to low estrogen levels. In turn, this suggests that the MCG, though not a self-sufficient site for the hormonal priming of lordosis, does modulate sexual motivation by mediating facilitatory effects of estrogen on receptivity and mating.

Animals↗
PubMed1990

The septum as origin of a lordosis-inhibiting influence in female rats: effect of neural transection.

The septum as the origin of a lordosis-inhibiting influence in female rats has been studied. Prior to testing, brain surgery was performed. Some rats were given a ventromedial cut (VMC) just above the anterior commissure, other rats, a posterior transverse cut (PC) or a dorsal horizontal cut (DC) just below the corpus callosum, and still other rats, a bilateral ventrolateral cut (VLC) in the ventrolateral septum and the bed nucleus of the stria terminalis (BST). Additionally, castrated females and those with a VLC sham operation served as castrated controls and sham-operated controls, respectively. All rats were given a daily dose of 0.2 micrograms of estradiol benzoate (EB) for three days and 0.5 mg of progesterone just prior to testing. The castrated controls evidenced no lordotic response. Lordotic activities also were very low in the surgically operated groups, with the exception of the VLC rats who demonstrated significantly high lordotic scores following the administration of 0.2 micrograms of EB. Two further testings, with the EB increased to 0.5 micrograms, were conducted, the interval between these tests being 2 weeks, and the VLC rats again demonstrated significantly higher lordotic activity than did the other rats. These results suggest that the septum exerts a lordosis-inhibiting influence, and that the ventrolateral outputs play a critical role in sending this inhibitory signal.

Amygdala↗
PubMed1991

Progesterone facilitates lordosis, but not LH release, in estradiol pulse-primed male rats.

Gonadectomized (GDX) male and female rats received repeated cycles of estradiol pulses, which prime animals of both sexes to display progesterone-facilitated lordosis. One, three and six treatment cycles of estradiol pulses followed by progesterone induced progressively higher luteinizing hormone (LH) surges in GDX females. Six treatment cycles of estradiol pulses alone (i.e., without subsequent progesterone treatment) induced a small but significant (approximately 4 ng/ml) increase in LH levels in GDX females. In contrast, GDX males never produced LH surges in response to estradiol pulses alone or estradiol pulses followed by progesterone, regardless of the number of hormone treatment cycles. Thus, female patterns of steroid-induced sexual receptivity and LH release are not inextricably linked, as steroid treatments sufficient for induction of lordosis do not stimulate LH secretion in adult male rats. These data also suggest that the neural system governing the LH surge might be more firmly sexually differentiated than that responsible for sexual receptivity in rats.

Animals↗
PubMed1992

Inhibition by N-methyl-D-aspartic acid (NMDA) receptor antagonist of lordosis behavior induced by estrogen followed by progesterone or luteinizing hormone-releasing hormone (LHRH) in the rat.

The effects of glutamate receptor antagonists on sexual receptivity induced by progesterone and LHRH were examined in ovariectomized, estradiol-primed rats (OVX-EB). Enhancement of lordosis/mounts quotient (L/M) by progesterone (0.5 mg) or LH-RH (150 ng; third ventricle, IVT) in OVX-EB rats was significantly decreased by IVT injection of (+) 2-amino-7-phosphonoheptanoic acid a competitive N-methyl-D-aspartic acid (NMDA) receptor antagonist. On the contrary, there were no changes in L/M quotient after IVT injection of 6,7-dinitroquinoxaline-2,3,dione at two dose levels, a Non-NMDA receptor antagonist. The NMDA antagonist did not modify lordosis behavior in OVX-EB rats. The results indicate that the NMDA type of glutamate receptors appears to mediate progesterone and LHRH facilitatory actions and suggest that glutamatergic synapses may be involved in lordosis-facilitating neural mechanisms.

2-Amino-5-phosphonovalerate↗