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PubMed1984

Dihydrotestosterone stimulates mounting behavior but not lordosis in female rats.

The ability of androgens to stimulate masculine sexual behavior is thought to depend on the aromatization of such androgens to estrogens. In this scheme, reduced androgens such as dihydrotestosterone (DHT) which cannot be aromatized, are thought to exert major peripheral but little or no central nervous system influences on the display of masculine sexual behavior. Further, an early report that DHT can induce lordosis, an estrogen (E) dependent behavior, led to a notion that DHT may effect behavior through metabolic intermediates such as 5 alpha-androstane-3 beta, 17 beta-diol (ADIOL) which then binds to estrogen receptors eliciting the E-dependent lordotic response. The present study reexamined and compared the relative effectiveness of a range of DHT dosages in stimulating a characteristic masculine (mounting) and feminine (lordosis) sexual behavior. Adult ovariectomized rats were randomly assigned to either 250 micrograms or 1 mg daily injections of DHT or DHTP. Other animals received OIL injections or crystalline DHT delivered by two different lengths (20 mm or 40 mm) of Silastic capsules. Animals were tested once weekly (for 5 weeks) for mounting behavior (20 minute test). Then animals were tested thrice (once weekly) for lordosis 4 hrs after the addition of 500 micrograms Progesterone (P). Finally, all females were tested for lordotic potential to respond to 10 micrograms EB plus P. 1 mg DHT or DHTP dosages and the 40 mm-Silastic condition significantly increased mounting behavior over that of lower dosages and OIL controls. A significant correlation existed between mounting frequency and circulating level of serum DHT. Treatment with DHTP was not different than DHT in eliciting mounting behavior.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effects of REM deprivation on the lordosis response induced by gonadal steroids in ovariectomized rats.

Ovariectomized rats were submitted to REM sleep deprivation (REMd) using the water tank technique and their behavioral responsiveness (lordosis) to gonadal steroids was tested. In Experiment 1, animals received 2 micrograms of estradiol benzoate (EB) followed by 2 mg of progesterone (P) 44 hours later. Several REMd periods (12, 72, 96 and 120 hr) were applied, all ending four hr after P. REMd animals showed significantly lower lordosis quotients (LQ) than undisturbed sleep animals regardless of the duration of the deprivation period. In Experiment 2, animals received a single dose of EB (2 micrograms) and were REMd for 120 hours. Animals were tested daily to evaluate their LQ. EB, at this dose level, failed to elicit significant lordosis behavior in undisturbed sleep rats. REMd rats gradually increased their LQ values reaching maximal levels at 72 hours. Adrenalectomized control groups receiving the same hormonal treatment responded similarly to the experimental groups, thus discarding the participation of adrenal steroids in these effects. The present results show that REMd differentially affects the response to E and P in ovariectomized rats, enhancing the former and inhibiting the latter.

Animals↗
PubMed1985

Effects of estrus, estrogen-progesterone priming, and vaginal stimulation on tonic immobility, dorsal immobility, and lordosis in the female rat.

Three complex inhibitory responses, tonic immobility, the dorsal immobility response, and lordosis, were studied in the intact female rat during estrus and diestrus and in ovariectomized rats with estrogen-progesterone treatment or controls. In each condition, the effects of vaginal-cervical stimulation were also studied. The results of two experiments indicate that estrus and estrogen-progesterone treatment significantly potentiate lordosis and the dorsal immobility response with or without vaginal-cervical stimulation. Tonic immobility was also potentiated by estrus and estrogen-progesterone treatment, but only if vaginal-cervical stimulation was applied. Vaginal-cervical stimulation potentiated both tonic immobility and the dorsal immobility response, but not lordosis, which was already at a high level.

Animals↗
PubMed1976

Stimulation of mounting behavior but not lordosis behavior in ovariectomized female rats by p-chlorophenylalanine.

Treatment with 126 mg/kg of the 5-hydroxytryptamine synthesis inhibitor p-chlorophenylalanine (PCPA) for 3 days or daily treatment with 40 mg/kg of PCPA stimulated the display of mounting behavior, including ejaculatory patterns, by ovariactomized hormonally untreated female rats. PCPA treatment failed to induce lordosis behavior and did not affect the induction of lordosis behavior by daily injections of 2.0 mug/kg estradiol benzoate. These results show that mounting and lordosis behavior can be dissociated and it is suggested that these two sexual behavior patterns may be regulated by different neurotransmission mechanisms.

Animals↗
PubMed1981

Antagonism of estrogen-induced lordosis by corticosterone in adrenalectomized-ovariectomized female rats and mice.

Previous experimentation has established that adrenalectomy can facilitate lordosis in ovariectomized estrogen-primed female rats. Experiment 1 examined the role of adrenal steroids in this effect, the results indicating an attenuation with chronic corticosterone but not with desoxycorticosterone or progesterone administration. Experiment 2 established a dose-response curve for this corticosterone effect. Experiments 3 and 4 indicated that corticosterone administration inhibits lordosis when it precedes estrogen administration. Experiment 5 demonstrated that corticosterone also inhibits estrogen-induced lordosis in mice. These data suggest that corticosterone may modulate estrogen-mediated behavior in rodents.

Adrenalectomy↗
PubMed1986

Harmine reverses the inhibition of lordosis by the 5-HT2 antagonists pirenperone and ketanserin in the female rat.

The beta-carboline harmine was found to facilitate lordosis behavior in ovariectomized rats primed with estradiol benzoate. Moreover, harmine reversed the inhibition of lordosis by the serotonin type 2 (5-HT2) antagonists pirenperone and ketanserin in rats primed with estradiol benzoate and progesterone. These results suggest that harmine facilitates lordosis by enhancing activity at 5-HT2 receptors.

Alkaloids↗
PubMed1986

Lordosis behavior and GABAergic neurotransmission.

gamma-Aminobutyric acid (GABA) (1.0 microgram/cannula) or muscimol (50 ng/cannula) was injected into the ventromedial hypothalamus or the lateral septi nuclei of ovariectomized rats brought to sexual receptivity by combined treatment of estrogen and progesterone. No inhibitory effects of GABA or muscimol were observed on the lordosis behavior. Furthermore, systemic (1.0 mg/kg) or intrahypothalamic (50 ng/cannula) picrotoxin administration was followed by a statistically significant increase in lordosis behavior in ovariectomized, estrogen-primed rats. No such effect was observed in ovariectomized-adrenalectomized animals, indicating its dependence on adrenal secretions. Present results do not support the hypothesis of a GABAergic mechanism in the hormonal control of lordosis behavior.

Adrenalectomy↗
PubMed1996

Ca2+/calmodulin system: participation in the progesterone-induced facilitation of lordosis behavior in the ovariectomized estrogen-primed rat.

We studied the effect some drugs that participate in the Ca2+/ calmodulin system have on the progesterone (P) facilitation of lordosis behavior in ovariectomized estradiol (E2) primed rats. We injected rats 44 h after E2 priming with 2 mg P together with various dosages of one of the following compounds: pentobarbital, trifluoperazine (TPZ), promethazine (PMZ), Chlorpromazine (CPZ), haloperidol (HAL), pimozide (PIM), and verapamil (VER). Then 4 h after treatment, animals were tested for sexual behavior, expressed as the lordosis quotient (LQ). All drugs at 4 mg/kg or higher inhibited lordosis, but only HAL, PIM, and VER were active at 1 mg/kg. The maximum level of activity was shown by PIM, although at the dose of 8 mg/kg no statistical differences were found between this compound and TPZ or HAL. Pentobarbital (25 mg/kg) showed no significant difference from saline-treated controls. The activity of the tested drugs on the facilitation of sexual behavior appears to be related to their efficiency as inhibitors of calmodulin (CaM)-dependent phosphodiesterase and as ligands for the Ca(2+)-CaM complex.

Animals↗
PubMed1995

Stria terminalis conveys a facilitatory estrogen effect on female rat lordosis reflex.

The effects of bilateral cut of the stria terminalis (ST) on the dosage of estradiol benzoate (EB) needed to induce the lordosis reflex in the ovariectomized female rat were examined. Seven different doses ranging 0.5-20 micrograms were given s.c. in oil, daily for 2 days in a counterbalanced order, at 3-week intervals. The log dose-response relationship was linear in both ST-cut and sham-operated control rats. A significantly larger dose of 9.3 +/- 1.4 (mean +/- SEM) micrograms/day of EB was needed in the ST-cut rats (n = 8) to obtain a 50% lordosis quotient than in the controls (n = 7), in which a 2.0 +/- 0.3 micrograms/day dose had a similar effect. The slope of the dose-effect curve was significantly steeper in the ST-cut rats than in the controls. The ST mediates facilitatory effects of estrogen on the lordosis reflex that originate presumably in the amygdala.

Animals↗
PubMed2004

Effect of estrogen on the lordosis-inhibiting action of ketanserin and SB 206553.

The effects of the 5-HT(2A/2C) receptor antagonist, ketanserin, and the 5-HT(2C) receptor antagonist, SB 206553, on lordosis behavior were investigated in ovariectomized rats hormonally primed with estradiol benzoate (EB) (0.5 or 25 microg) and progesterone (500 microg). Both ketanserin and SB 206553 inhibited lordosis behavior after infusion into the ventromedial nucleus of the hypothalamus (VMN), but ketanserin was slightly more effective than the 5-HT(2C) receptor antagonist. Either drug was more effective in rats primed with 0.5 microg EB than in rats hormonally primed with 25 microg EB. These findings support the suggestion that estrogen may enhance functioning of the 5-HT(2) receptor family and thereby protect against the 5-HT(2) receptor antagonists. These data are consistent with prior suggestions that estrogen modulates functioning of 5-HT(2) receptors within the VMN and that 5-HT(2) receptors play a facilitatory role in the modulation of female rat lordosis behavior.

Analysis of Variance↗
PubMed2004

WAY100635 and female rat lordosis behavior.

Sexually receptive proestrous rats with bilateral cannulae in the ventromedial nucleus of the hypothalamus (VMN) were infused with 200 ng of (+/-)-8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) or with 8-OH-DPAT plus varying concentrations (200 to 2000 ng) of the 5-HT1A receptor antagonist, N-[2[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]N-(2-pyridinyl)cyclohexanecarboxamide trihydrochloride (WAY100635). 8-OH-DPAT inhibited lordosis behavior within 15 min of the infusion and every dose of WAY100635 prevented the inhibition. When non-sexually receptive, ovariectomized rats, hormonally primed with 0.5 microg estradiol benzoate and 500 microg progesterone, were infused with WAY100635 (400 to 2000 ng), the 5-HT1A receptor antagonist did not facilitate lordosis responding. These findings support earlier findings that activation of 5-HT1A receptors in the mediobasal hypothalamus inhibits lordosis behavior. However, they further demonstrate that tonic activation of 5-HT1A receptors is not responsible for the absence of sexual receptivity in suboptimally hormonally primed ovariectomized rats.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2001

Inhibition of lordosis behavior by intrahypothalamic infusion of a protein kinase G antagonist.

Previous experiments demonstrated that intracerebroventricular infusion of the protein kinase G inhibitor KT5823 inhibits lordosis behavior in hormone-treated female rats. Present studies show that KT5823 attenuates lordosis in a dose-dependent manner when infused bilaterally into the ventromedial hypothalamus. Thus, activation of protein kinase G in the ventromedial hypothalamus is necessary for the expression of hormone-dependent lordosis behavior in female rats.

Alkaloids↗
PubMed1997

Effects of an intrahypothalamic injection of antisense oligonucleotides for preproenkephalin mRNA in female rats: evidence for opioid involvement in lordosis reflex.

Previous studies in female rats have shown that estrogen increases preproenkephalin (PPE) mRNA levels in the ventrolateral part of the ventromedial nucleus of the hypothalamus (VMHVL), an area implicated in the modulation of sexual behavior. In order to assess the physiological role of hypothalamic opioid expression in lordosis reflex 16-mer oligodeoxynucleotide (ODN) directed towards the PPE mRNA were acutely microinjected above the VMH of estradiol-primed ovariectomized rats. Estradiol-induced lordosis behavior was observed in response to a stud male 2 days thereafter. Antisense (without or with 4 mismatches) ODN injections near the VMHVL resulted in a significant reduction in lordosis quotient compared to control (reverse sense) ODN treatment or to antisense ODN injections targeted anterior or posterior to the VMHVL. In contrast, locomotor activity of these animals in the open-field test was not affected by ODN treatments. Enkephalin immunoreactive levels were determined by radioimmunoassay in the preoptic area, a major terminal field of the VMHVL. Estradiol-induced enkephalin levels were greatly reduced in antisense-treated groups. Using the in situ hybridization technique, PPE mRNA levels in the VMHVL were also determined. A 1.5-2-fold increase in PPE mRNA levels was observed in estradiol-treated rats compared to ovariectomized rats as previously described. This increase in PPE mRNA levels was not affected by ODN treatment, suggesting that the reduction of enkephalin expression was mainly due to physical blockade of PPE mRNA translation and not to its degradation. Taken together, these data further support the behavioral role of PPE expressing VMHVL neurons. They also highlight the in vivo potency of acute administration of antisense phosphorothioate ODNs in blocking neuronal target gene expression.

Amino Acid Substitution↗
PubMed1998

Separation of septal influences on lordosis, ultrasound production, and body weight.

Previous results suggest that septal fibers inhibit lordosis, ultrasound production, and bodily growth (rate of weight gain) in female hamsters. To determine if the systems responsible for these effects can be dissociated, septal connections with or through the preoptic area (POA) were disrupted by horizontal cuts across the interface between these areas. Some subjects received cuts that were centered medially and extended across most of the interface. Others received cuts that were offset laterally and disrupted just the lateral half of this region. Each response was affected by at least one of these cuts. However, the patterns of effects differed across measures. Lordosis was facilitated equally by medial and lateral cuts, suggesting its dependence on fibers that are concentrated where the cuts overlapped, i.e., laterally along the septal-POA interface. In contrast, ultrasound rate was increased just by the more medial cuts, suggesting its dependence on relatively medial fibers. Finally, body weight was increased by both lesions but consistently responded more to the more medial cuts. This suggests that the relevant fibers are distributed across much of the septal-POA interface but are concentrated in its medial half. Taken together, these results suggest that septal connections affecting lordosis, ultrasound production, and body weight follow different trajectories as they enter or leave the ventral septum. In turn, this strengthens the case for the mediation of these effects by distinct populations of septal cells.

Animals↗
PubMed2000

Factors elevating cAMP attenuate the effects of 8-OH-DPAT on lordosis behavior.

The effects of a soluble derivative of forskolin and of two membrane-permeable analogs of cAMP, dibutyryl cAMP, and 8-bromo-cAMP, on the ability of a serotonin (5-HT)(1A) receptor agonist to inhibit lordosis behavior were examined. Sexually receptive, proestrous rats received a bilateral infusion into the ventromedial nucleus of the hypothalamus (VMN) with 68 ng of the forskolin derivative 1, 1.5, 2, or 2.5 h prior to infusion with 200 ng of the 5-HT(1A) receptor agonist, (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). Proestrous rats and ovariectomized rats, hormonally primed with 25 microg estradiol benzoate and 500 microg progesterone, were coinfused with 200 ng 8-OH-DPAT and either 50 microg dibutyryl cAMP or 5 microg 8-bromo-cAMP. In proestrous rats, prior infusion with the forskolin derivative reduced the effects of the 5-HT(1A) receptor agonist on lordosis behavior. The best protection occurred at 2 h; by 2.5 h after the preinfusion, any protective effect had disappeared. Coinfusion with either dibutyryl-cAMP or 8-bromo-cAMP reduced the effects of 8-OH-DPAT in proestrous rats. In hormone-primed, ovariectomized rats, dibutyryl cAMP offered significant protection against the effects of 8-OH-DPAT, but there was no protection with 8-bromo-cAMP. These findings are consistent with the speculation that 8-OH-DPAT's inhibition of lordosis behavior results, in part, from an inhibition of adenylyl cyclase, resulting from agonist activation of 5-HT(1A) receptors in the VMN. The findings are also consistent with our earlier observations for differences between proestrous rats and hormone-primed, ovariectomized rats in their response to 5-HT receptor-active compounds.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1984

Cholecystokinin-octapeptide produces inhibition of lordosis in the female rat.

The peripheral administration of 3 micrograms/kg CCK-8 produced inhibition of lordosis behavior in ovariectomized female rats primed with estradiol benzoate (EB) and progesterone (P). In Experiment 2, an interaction between CCK-8 and P was evident, with the inhibitory effects of CCK-8 being observed with P doses of 100 and 150 micrograms, but not 250 micrograms. No interaction between CCK-8 and EB was evident, as CCK-8 had no effect on lordosis behavior induced by chronic administration of EB alone. The ineffectiveness of CCK-8 in animals treated with high doses of P, or EB administered chronically, suggests that CCK-8 does not inhibit lordosis via a toxic or non-specific mechanism.

Animals↗
PubMed1997

beta-endorphin inhibits and facilitates lordosis behaviour in rats depending on ventricular site of administration.

beta-endorphin was administered intracerebroventricularly into the lateral and third ventricles of ovariectomized, oestrogen- and progesterone-primed rats, and its effect on lordosis and ear-wiggling was assessed. A dose of 2 micrograms beta-endorphin facilitated lordosis when infused into the lateral ventricle, but inhibited lordosis when infused into the third ventricle. The effects were the same whether measured at 30, 60 or 90 min following infusion. beta-endorphin had no significant effect on ear-wiggling frequency when administered in either ventricle. The differential effects of beta-endorphin depending on site of administration may reflect the activation of distinct opioid receptor subtypes within the brain.

Analysis of Variance↗
PubMed1993

Brain monoaminergic neurotransmission in the mediation of lordosis behavior in the female rat.

The present paper reviews recent pharmacological evidence indicating an important role for central monoaminergic neurotransmission in the mediation of lordosis behavior in the female rat. Following the initial observations by Meyerson and his colleagues in the early 1960s, demonstrating an inhibitory serotonergic mechanism, continued studies have identified 5-hydroxytryptamine (5-HT) 5-HT1A receptors to be of particular importance. Stimulation of central 5-HT2 receptors appear to have an opposite role, i.e. facilitating the elicitation of the lordosis response. As regards brain dopaminergic neurotransmission, it appears that brain dopamine (DA) D2 receptors mediate an inhibitory effect on the lordosis behavior, whereas no distinct role has been ascribed to DA D1 receptors. The serotonergic and the dopaminergic mechanisms can be manipulated independently, perhaps indicating the operation of parallel mechanisms. Most of the evidence presented above has been obtained in experiments on ovariectomized female rats primed with subthreshold doses of estrogen. It appears, however, that at least the inhibitory effects mediated by serotonergic neurotransmission are not dependent on the presence of progesterone.

Animals↗