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PubMed1983

Effects of serotonin agonists on lordosis, myoclonus, and cytoplasmic progestin receptors in guinea pigs.

Peripheral treatment with the serotonin releaser fenfluramine or the serotonin agonist quipazine abolished lordosis behavior in ovariectomized estradiol and progesterone-primed female guinea pigs. Quipazine was also effective when administered into a lateral cerebral ventricle. The lowest dose of fenfluramine that induced myoclonus (10 mg/kg) was higher than the dose needed to inhibit lordosis (5 mg/kg). Therefore, it appears that myoclonus and lordosis are differentially sensitive to serotonin agonists. The effects of quipazine on lordosis were time dependent. Quipazine had no effect on lordosis when given prior to the onset of sexual receptivity. These data suggest that serotonin agonists might be effective only when progesterone has had sufficient time to induce sexual receptivity. Quipazine did not affect cytoplasmic progestin receptors in brain areas involved in steroid hormone effects on lordosis. This finding, and the finding that quipazine had no effect on lordosis when given prior to the onset of sexual receptivity, suggest increased serotonin transmission does not interfere with estrogen priming or sensitivity of hypothalamic cells to progesterone.

Animals↗
PubMed1988

Progesterone facilitation of lordosis in male and female Sprague-Dawley rats following priming with estradiol pulses.

Adult male Sprague-Dawley rats rarely exhibit progesterone-facilitated lordosis following steroid treatments which are effective in females. In contrast, progesterone-facilitated lordosis has been observed following priming with estradiol pulses in another strain. The aim of this study was to compare progesterone-facilitated feminine sexual behavior in adult male and female Sprague-Dawley rats following priming with estradiol benzoate (EB) or estradiol pulses. Female sexual behavior was measured in adult, gonadectomized males and females treated as follows: Two pulses of estradiol followed by progesterone or oil the next day; EB (two doses) for 3 days, and progesterone or oil the next day. These protocols were repeated at 4- or 6-day intervals, respectively. Progesterone-facilitated lordosis was observed consistently in both sexes treated with estradiol pulses. By the fifth test, lordosis quotients did not differ between the sexes, but the lordosis ratings in progesterone-treated males remained lower than those observed in females. Proceptivity (hop-darting) was facilitated by progesterone in females, but was never observed in males. Lordosis was induced in both sexes by 15 micrograms EB, but was not reliably facilitated by progesterone. Treatment with the lower dose of EB (1.5 micrograms) induced high levels of receptivity in females (occasionally facilitated by progesterone), but not in males regardless of subsequent treatment (i.e, progesterone or oil). These data suggest that progesterone-facilitated lordosis can be induced in male Sprague-Dawley rats, if a regimen of estradiol pulses is used. Thus, the brain of the adult male is not inflexibly differentiated with regard to progesterone facilitation of feminine receptive behavior.

Animals↗
PubMed1989

Development of steroid-induced lordosis in female guinea pigs: effects of different estradiol and progesterone treatments, clonidine, and early weaning.

The ability of developing ovariectomized (OVX) guinea pigs to display lordosis following a variety of steroid treatments which are behaviorally effective in adults was examined. Females OVX at 11 days of age did not display lordosis at 20 days of age, following treatment with several dose combinations of estradiol benzoate (EB, 10-50 micrograms) and progesterone (0.5-5 mg). By 30 days of age, 25% of the animals responded to EB plus progesterone, and by 40 days of age, adult-typical responses were observed. The developmental profile of responsiveness to steroids was not altered by varying the age at OVX, or by allowing pups to remain with a lactating mother. OVX females given estradiol (E2) implants did not exhibit progesterone-facilitated lordosis earlier than those treated with EB: however, the former group did show an unusually high incidence of progesterone-independent lordosis at 40 days of age. Twenty-day-old females also did not respond behaviorally to discrete pulses of E2 followed by progesterone, a treatment which was very effective in adults. Finally, lordosis was not facilitated in EB-primed, 20-day-old females by the alpha-noradrenergic agonist, clonidine, a treatment which was effective in adult females. These data illustrate a variety of conditions under which juvenile female guinea pigs do not exhibit steroid-induced lordosis. Since 20-day-old, EB-treated females also did not exhibit clonidine-facilitated lordosis, incomplete development of the central steroid-responsive and/or noradrenergic systems may contribute to the inability to display steroid-induced estrous behavior at this age.

Animals↗
PubMed1990

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.

Androstatrienes↗
PubMed1991

Morphine suppresses the ovarian steroid hormone-dependent lordosis response of female guinea pigs: reversal by naloxone but not clonidine.

The opiate agonist morphine caused a dose- and time-dependent suppression of lordosis responding in ovariectomized guinea pigs treated with estradiol-17 beta and progesterone. The suppression of lordosis by morphine appears to be mediated by opiate receptors since the opiate antagonist naloxone blocked its effects both in terms of the percentage of animals showing lordosis and the duration of individual responses. Naloxone, when given alone, did not affect lordosis responding in estradiol-17 beta + progesterone-primed animals and did not induce lordosis in animals primed with estradiol-17 beta alone. Thus, endogenous opioids might not tonically inhibit lordosis under the physiological conditions examined. The alpha-noradrenergic agonist clonidine did not reverse the effects of morphine on lordosis. Thus, the inhibitory effects of morphine on this behavior might be independent of its presynaptic effects on norepinephrine release in brain.

Animals↗
PubMed1982

Dissociation between the display of lordosis and soliciting behaviors in female rats with lesions of the dorsomedial pontine tegmentum.

Lesions of the dorsomedial tegmentum (DMTL) between the midbrain pontine junction and the middle level of the pons effectively eliminate the induction by estrogen-progesterone of lordosis behavior in ovariectomized rats. However, soliciting behaviors such as ear wiggling and hopping were not inhibited by this type of lesion. The common damaged area in DMTL rats which failed to show lordosis was the medial periventricular gray. The lesions placed in the caudal pontine central gray were not effective in suppressing lordosis response. Lesions of the ventromedial tegmentum (VMTL) were also ineffective in suppressing lordosis. Most of the animals with the VMTL showed soliciting behaviors. In these rats, the incidence of lordosis and lordosis quotient (LQ) were comparable to those of sham operated rats. When bilateral lesions were placed in the lateral tegmentum region, the mean LQ and incidence of soliciting behavior were not significantly different from those of sham operated controls. These results suggest a clear dissociation of the regulatory mechanisms between the display of lordosis and soliciting behaviors at the pontine level.

Animals↗
PubMed1983

Impairment or abolition of lordosis in the golden hamster by transection of spinal pathways.

Lumbosacral and thoracic tactile stimulation elicits lordosis in sexually-receptive female hamsters. Because of the major dorsal column involvement in transmission of tactile activity, transection of this pathway was examined for effects on somatosensory elicitation of lordosis and compared with effects of lateral column (unilateral or bilateral) transections. Interruption of either pathway completely eliminated lordosis on some tests. Dorsal column section at cervical or lumbar levels produced a unique effect, however, where lumbosacral stimuli elicited the tail, rump and hindlimb manifestations of lordosis without evoking the usual immobility of the forelimbs, head and vibrissae. In animals with lumbar transections, the rostral, but not caudal, motoric components of lordosis could still be elicited by thoracic stimuli. Lateral column transection did not consistently prevent complete, sustained lordosis responses, but the response posture was abnormal. These results show the integrity of the hamster's dorsal columns to be essential for elicitation of complete lordosis responses and suggest that the caudal and rostral motor components differ significantly in the nature of their control by spinal and supraspinal levels of the central nervous system.

Afferent Pathways↗
PubMed1984

Administration of estradiol-17 beta in pulses to female guinea pigs: self-priming effects of estrogen on brain tissues mediating lordosis.

Lordosis behavior in ovariectomized guinea pigs is facilitated by the sequential action of estradiol-17 beta (E) and progesterone (P). The present study was designed to explore the possibility that administration of E in a pulsatile manner is more efficacious than a single injection of E with respect to lordosis facilitation in ovariectomized guinea pigs. The data indicate that pulse administration of unesterified E is more effective than a single large dose of E for the facilitation of lordosis behavior. Three injections of as little as 0.5 microgram E at 0, 19 and 28 hr followed by 0.5 mg P at 39 hr was more effective (63.6% responding with lordosis) than a single injection of as much as 15 micrograms E at hr 0 followed by vehicle injections at 19 and 28 hr and 0.5 mg P at 39 hr (0% responding). We also demonstrated that the 19 hr E injection could be eliminated and that two injections of E (0.5 microgram at hr 0 and 1.0 microgram at hr 28 followed by 0.5 mg P at hr 39) was at least as effective (69.0% responding) as three split injections in facilitating lordosis. This behaviorally effective pulse administration of E also resulted in significant induction of cytoplasmic progestin receptors in hypothalamic tissue. Further experiments indicated that a 28 hr interval between E pulses was optimal in terms of percent animals displaying lordosis. The data suggest that pulsatile E stimulation of brain tissues mediating lordosis is a highly effective mode of stimulation, and that an initial pulse of E sensitizes neural tissues to subsequent E administration.

Animals↗
PubMed1989

Effects of site-specific CNS microinjection of cholecystokinin on lordosis behavior in the male rat.

We have previously demonstrated that intracerebroventricular injections of sulphated cholecystokinin octapeptide (sCCK-8) had a dramatic facilitatory effect on lordosis behavior in the gonadectomized, estrogen-primed male rat. In the female, sCCK-8 facilitates or inhibits lordosis when microinjected into the medial preoptic nucleus (MPN) or ventromedial nucleus of the hypothalamus (VMH), respectively. In order to identify sCCK-8 responsive sites that modulate lordosis behavior in gonadectomized males, sCCK-8 was microinjected into the MPN or VMH. Sulphated CCK-8 significantly increased lordosis behavior when microinjected into the MPN of estrogen-primed males, but had no significant effects when microinjected into the VMH. These results imply that CCK-sensitive neural substrates within the MPN may act to disinhibit lordosis in the gonadectomized, estrogen-primed male rat. The lack of an effect of VMH injection of sCCK-8 on lordosis in males is discussed in terms of possible sex differences in sCCK-8-sensitive lordosis-modulating circuits.

Animals↗
PubMed1990

Intrahypothalamic implants of noradrenergic antagonists disrupt lordosis behavior in female rats.

There is considerable experimental evidence that hormonal activation of lordosis in female rats involves norepinephrine (NE) neurotransmission. However, no clear picture has emerged regarding either: 1) the neural sites at which NE influences lordosis, or 2) the NE receptor subtype(s) mediating NE effects on lordosis. To address these two issues, the behavioral effects of antagonists with relative specificity for alpha 1, alpha 2, or beta adrenergic receptors were examined. Drugs were administered via bilateral crystalline implants directly into the ventromedial nucleus of the hypothalamus (VMN) or medial preoptic area (MPOA) of ovariectomized female rats primed for 48 hr with 3 micrograms of estradiol benzoate (EB) and given 200 micrograms of progesterone (P) 3.5-4 hr before testing. When applied to the VMN 1 hr before the P injection, the alpha 1 receptor antagonist prazosin reduced lordosis behavior in 86% of animals but in only 10% of rats when applied to the MPOA. However, prazosin did not inhibit lordosis when implanted into the VMN just prior to EB administration. Yohimbine, an alpha 2 receptor antagonist with low affinity for alpha 1 receptors, also suppressed lordosis in 41% of animals with VMN implants and in 37% of rats with MPOA implants. By contrast, the alpha 2 antagonist idazoxan, which has little activity at alpha 1 receptors, did not significantly affect estrous responding when implanted into either the VMN or MPOA. VMN implants of the beta receptor antagonists propranolol and pindolol reduced lordosis behavior in 50% and 86% of rats, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Interruption of the lordosis reflex of female rats by ventral midbrain stimulation.

The lordosis reflex, dorsiflexion of the vertebral column, is an estrogen-dependent, essential element of female sexual behavior in rodents. Unilateral electrical stimulation of the midbrain ventral tegmental area through a chronically implanted electrode in freely moving, estrogen-primed ovariectomized female rats caused a rapid and strong suppression of the lordosis reflex in response to either male mounts or manual cutaneous stimuli. The interruption occurred in a graded manner to increased stimulus intensity, with a threshold at 30 microA. The optimal frequency was at 75-125 Hz. After the termination of electrical stimulation, lordosis performance returned promptly to the pre-stimulation level. No aversive response accompanied the blockade of lordosis. Electrical stimulation specifically blocked lordosis, without disrupting the proceptive components of female sexual behavior. In 10 animals tested, concomitant injection of dopamine receptor blocker pimozide tended to offset the effects of electrical stimulation in 2 cases. Interruption of the lordosis reflex might be mediated by projections from the ventral tegmental area, which activate a descending pathway inhibitory to the lordosis reflex arc at or below the lower brain stem.

Afferent Pathways↗
PubMed1985

Prevention of progesterone-induced lordosis behavior by alpha or beta adrenergic antagonists in ovariectomized estrogen-primed rats.

The effect of systemic administration of adrenergic alpha (phenoxybenzamine and prazosin) and beta (propranolol) antagonists on the lordosis behavior induced by progesterone (2.0 mg/rat) was studied in ovariectomized estradiol benzoate (4.0 micrograms/rat) primed rats. The effect of these antagonists was also tested on the lordosis behavior induced in ovariectomized rats by estradiol benzoate alone (1.25 micrograms/rat each two days). Phenoxybenzamine (0.8, 4.0 and 20.0 mg/kg), propranolol (0.8, 4.0 and 20.0 mg/kg) and prazosin (0.2 and 1.0 mg/kg) caused a dose-dependent reduction of progesterone induced lordosis. By contrast, phenoxybenzamine (4.0 mg/kg), propranolol (4.0 mg/kg) or prazosin (1.0 mg/kg) did not affect estrogen induced lordosis behavior. Results suggest the following conclusions: (1) blockage of either alpha or beta adrenoreceptors prevents progesterone induced lordosis behavior and (2) the adrenergic neuron involved in progesterone facilitation of lordosis behavior is not a part of the reflex arc for lordosis but probably modulates the activity of this system.

Adrenergic alpha-Antagonists↗
PubMed1986

Norepinephrine infusions into the medial preoptic area inhibit lordosis behavior.

Neurotransmitters, including norepinephrine, have been implicated in the mediation of ovarian steroid induced lordosis behavior in ovariectomized rats. In this study we have found that norepinephrine (NE) infusions into the medial preoptic area (MPOA) reduced lordosis frequencies of estrogen-progesterone treated (0.5 micrograms estradiol benzoate for three days followed by 500 micrograms progesterone 4-5 hours before testing) receptive rats. Norepinephrine doses of 2 micrograms or more per animal infused into the MPOA significantly reduced lordosis levels within five minutes. Infusions of 10 and 20 micrograms doses of NE suppressed lordosis levels for 15 minutes after infusion. At the lowest inhibitory dose (2 micrograms/animal) simultaneous infusion of 5 micrograms/microliter of the noradrenergic antagonist yohimbine, but not of phentolamine or propranolol, blocked the reduction in lordosis resulting from NE infusion. Preoptic infusions of epinephrine and clonidine were also effective in reducing lordosis quotients, while methoxamine, phenylephrine and isoproterenol did not alter receptivity. These findings are consistent with the conclusion that the direct effect of norepinephrine infusions into the MPOA is inhibition of lordosis responding. There is some evidence that this inhibitory influence is mediated by alpha 2-noradrenergic receptors.

Animals↗
PubMed1988

Possible role of inhibitory glycinergic neurons in the regulation of lordosis behavior in the rat.

Strychnine sulfate (3.9 or 27 micrograms in 0.5 microliter saline) was bilaterally infused into the ventromedial hypothalamic nucleus (VMH) of ovariectomized sexually inexperienced rats primed 40 hr earlier with 4 micrograms of estradiol benzoate (EB). This dose of EB induced only weak lordosis behavior in 25% of the subjects (Ss). Strychnine at the 3 and 9 micrograms dosages, but not at 27 micrograms, induced intense lordosis behavior, but no proceptivity, in most estrogen-primed Ss (69% in 3 micrograms, 94% in 9 micrograms). Ovariectomized adrenalectomized EB-primed Ss also displayed significant lordosis behavior (59%) following infusion of 9 micrograms of strychnine into the VMH. Strychnine (9 micrograms) failed to stimulate lordosis in ovariectomized Ss that were not estrogen-primed. Administration of 5 micrograms EB followed 40 hr later by 2 mg of progesterone (P) elicited intense lordosis behavior in most Ss. Bilateral injections into the VMH of glycine (100 micrograms), beta-alanine (100 micrograms) or taurine (50 micrograms) to rats that were already displaying estrous behavior (greater than 80 LQ) in response to the sequential administration of EB and P failed to depress lordosis when tested between 5 min and 60 min postinjection. Similarly, glycine (20 or 100 micrograms) injected into the VMH of estrogen-primed, ovariectomized rats within 15 minutes of a 2 mg SC injection of P failed to interfere with the subsequent response to this steroid when tested 2 and 4 hr after P. The results suggest that strychnine injected into the VMH facilitates lordosis behavior in estrogen-primed rats by removing a tonic inhibitor effect exerted by glycinergic neurons on VMH neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

8-OH-DPAT in the midbrain central gray inhibits lordosis behavior.

Sexually receptive female rats were infused intracranially with 500-2,000 ng 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) into the midbrain central gray (MCG), in the vicinity of the dorsal raphe nucleus (DRN), or directly into the DRN. When cannulae were located within the DRN, there was little evidence of change in lordosis behavior but a decrease in locomotor activity was commonly observed. In contrast, when cannulae were located anterior, ventromedial, or lateral to the DRN inhibition of lordosis behavior was rapid and robust. Both the lordosis-to-mount ratio (L/M) and the quality of the lordosis reflex were reduced following the infusion. The MCG receives lordosis-facilitating input from the ventromedial nucleus of the hypothalamus and from ascending sensory pathways and contributes information to descending motor systems involved in the lordosis response. Thus, the MCG is a critical link in the completion of the estrogen-dependent lordosis reflex. The present results suggest that 5-hydroxytryptamine1A receptors in the MCG prevent the completion of this reflex.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1994

Estrogen dependence of cholinergic systems that regulate lordosis in cycling female rats.

Previous evidence indicated that physostigmine, an acetylcholinesterase inhibitor, facilitated lordosis behavior when administered intraventricularly to cycling female rats on proestrus prior to the onset of natural sexual receptivity, but not when administered to rats on mid-diestrus or diestrus II. In the present experiments, intraventricular infusion of physostigmine (10 micrograms bilaterally) facilitated lordosis on mid-diestrus and diestrus II if females were primed with two injections of estradiol (0.2, 0.1, or 0.05 micrograms) administered 20 h and 32 h prior to infusion of physostigmine. Despite unequal levels of endogenous progesterone, physostigmine facilitated lordosis equally on mid-diestrus and diestrus II following estradiol priming. Finally, intraventricular infusion of the muscarinic receptor blocker scopolamine (20 micrograms bilaterally) reduced the incidence of lordosis in females that displayed lordosis on mid-diestrus following estrogen priming. Results confirm that cholinergic mechanisms influence sexual behavior displayed by cycling female rats. Data further indicate that sufficient estrogen stimulation is necessary for cholinergic neurons to facilitate lordosis. However, progesterone does not play a major role in the regulation of lordosis by cholinergic systems.

Animals↗
PubMed1994

Roles of second-messenger systems and neuronal activity in the regulation of lordosis by neurotransmitters, neuropeptides, and estrogen: a review.

Many neurotransmitters and neuropeptides can affect the rodent feminine sexual behavior, lordosis, when administered in the ventromedial hypothalamus (VMH), midbrain central gray (MCG), or other brain regions. A survey of the electrophysiological and biochemical actions of these neural agents revealed that there is a very consistent association between lordosis facilitation with both the activation of the phosphoinositide (PI) pathway and the excitation of VMH and MCG neurons. In contrast, lordosis inhibition is associated, less consistently, with alterations of the adenylate cyclase (AC) system and the inhibition of neuronal activity. The findings that lordosis could be facilitated by going beyond membrane receptors and directly activating the PI pathway, suggest that this second-messenger pathway is a common mediator for the lordosis-facilitating agents. Furthermore, as in the case of stimulating membrane receptors, direct activation of this common mediator also requires estrogen priming for lordosis facilitation. Therefore, it is likely that the PI pathway is modulated by estrogen in the permissive action of estrogen priming. Indeed, a literature review shows that estrogen can affect selective isozymes of key enzyme families of the PI pathway at various levels. Such selective modulations, at several levels, could easily alter the course of a PI cascade; thence, the eventual functional outcome. These findings prompt us to propose that estrogen enables lordosis to be facilitated by a selective modulation of the PI pathway.

Animals↗
PubMed1989

Lateralized effects on hamster lordosis of unilateral hormonal and somatosensory stimuli.

To better describe the hypothalamic efferents that mediate estrogenic effects on lordosis, each of 18 ovariectomized hamsters received a 30 gauge implant of estradiol aimed at the right or left ventromedial hypothalamus (VMN). Six days later, subjects were treated with progesterone and observed for their durations of lordosis during brief periods with sexually-active males. Subsequently, the male was removed, as light manual stimulation was applied to the flank ipsi- or contralateral to the implant in attempts to (a) maintain as yet unbroken lordosis responses, or (b) reinstate lordosis in females showing limb movements indicative of their emergence from the male-elicited posture. The results failed to show any difference in the behavioral effects of implants aimed at the right versus left VMN. However, implants did interact selectively with manual stimulation of the ipsi- and contralateral flanks. Specifically, lordosis responses were more likely, more rapid, and better maintained to stimulation of the contralateral flank. This lateralization of the priming effect derived from a VMN estradiol implant is impressive for its persistence, and for its consistency with the trajectories of VMN efferents to the midbrain and of midbrain afferents from the flanks. The consistency of these behavioral and neuroanatomical patterns suggests that lordosis depends on direct interactions of the VMN and dorsal midbrain. In turn, it implicates the dorsal midbrain in the mediation on VMN-initiated hormonal effects on lordosis, and in the eventual integration of hormonal and somatosensory influences on sexual receptivity.

Afferent Pathways↗