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At least 415 records · Page 23Linked to original sources
PubMed1993

Role of perinatal estrogens in sexual differentiation of the inhibition of lordosis by exogenous cholecystokinin.

Microinjections of sulphated cholecystokinin octapeptide (sCCK-8) into the ventromedial nucleus of the hypothalamus inhibit lordosis behavior in receptive female rats. This effect of sCCK-8 seems to differentiate under the control of gonadal steroids shortly after birth. Neonatally castrated males and normal females show similar responses, while androgenized females are less sensitive to sCCK-8. The current study investigated estrogen's role on the differentiation of the response to sCCK-8. On the day of birth male rat pups were castrated, given sham surgeries, or implanted with the antiestrogen tamoxifen or the aromatase inhibitor androst-1, 4, 6-triene-3, 17-dione (ATD). Females were implanted with testosterone propionate or tamoxifen, or given sham surgeries. Implants were removed 10 days later. As adults, rats were tested for female sexual behavior after microinjections of sCCK-8 into the ventromedial nucleus of the hypothalamus. Neonatally castrated males, ATD-treated males, and control females showed profound inhibition of lordosis behavior after sCCK-8. These results suggest that elimination of estrogen postnatally prevents defeminization of the reproductive circuitry that responds to sCCK-8.

Androstatrienes↗
PubMed1978

Lordosis induction in the rat by prostaglandin E2 systemically or intracranially in the absence of ovarian hormones.

Within 20 minutes of an intraperitoneal injection, PGE2 induced lordosis responding to manual stimulation in 6 of 9 rats that were ovariectomized-hysterectomized and hormonally untreated. Similarly, intracranial application of PGE2, through guide cannulae that were chronically-implanted in the basal hypothalamus, induced lordosis responding to manual stimulation within 10 minutes in ovariectomized, hormonally-untreated rats.

Animals↗
PubMed1977

The influence of alpha-receptors on lordosis in the female rat.

The alpha-adrenergic agonist clonidine suppressed lordotic responding in spayed female rats brought into heat by estrogen and progesterone. The suppression was blocked by the alpha-antagonist yohimbine, but not by phenoxybenzamine or pimozide. The suppression was blocked by the alpha-antagonist yohimbine, but not by phenoxybenzamine or pimozide. Phenoxybenzamine itself had no suppressive effect on lordosis, though yohimbine did under some conditions. These results argue against an important facilitatory influence of norepinephrine on lordosis in the rat. Further, in comparison with the quite different findings recently reported from the guinea pig, they offer support for the presence of two different kinds of alpha-adrenergic receptors in the brain with different physiological functions.

Animals↗
PubMed1978

Biphasic effects of the antiserotonergic methysergide on lordosis in rats.

As also reported by other workers, the antiserotonergic drug methysergide was found to facilitate lordotic responding in estrogen primed, ovariectomized rats. A second dose of methysergide 24 hr after the first, however, failed to produce any increment in responding. Animals received daily estrogen injections in order to maintain a relatively constant level of priming. After several days of methysergide, a progesterone injection facilitated lordosis to the same degree as in controls receiving only saline and estrogen. When a second injection of progesterone was given 24 hr later, however, the animals failed to respond. In contrast, saline controls with this estrogen paradigm responded equally well to both progesterone injections. These results are discussed in terms of their bearing on possible serotonergic and non-serotonergic mechanisms by which progesterone may control lordosis.

Animals↗
PubMed1982

Dihydrotestosterone-induced inhibition of lordosis in estrogen-primed ovariectomized rats following 6-hydroxydopamine or electrolytic septal lesions.

The dose-dependent inhibition of lordosis by 5 alpha-dihydrotestosterone propionate in ovariectomized female rats treated concurrently with estradiol benzoate was attenuated neither by intracranial 6-hydroxydopamine injections which reduced dopamine concentrations by approximately 70% in septum or 75% in both septum and n. accumbens septi nor by electrolytic destruction of the lateral or medial septal nuclei or of both septal nuclei. These results suggest that inhibitory effect of dihydrotestosterone on estrogen-induced lordosis does not critically depend on the mesolimbic dopaminergic innervation of the forebrain or on the septal nuclei.

Animals↗
PubMed1990

Physostigmine facilitation of lordosis in naturally cycling female rats.

Both systemic and intracerebral administrations of the cholinergic muscarinic antagonist, scopolamine, have been shown to inhibit naturally occurring sexual behavior in intact, cycling female rats. The present study examined the facilitative effects of the acetylcholinesterase inhibitor, physostigmine (eserine), on sexual behavior in intact, cycling female rats. Cycling was determined by daily monitoring of sexual behavior and vaginal cytology. When administered during either early proestrus or proestrus, physostigmine activated lordosis 15 min and 1 hr after intraventricular infusion (10 micrograms bilaterally). However, infusion of physostigmine failed to facilitate lordosis 15 min after administration during either diestrus I, mid-diestrus, or diestrus II. The administration of this cholinergic agent did not interrupt cyclicity patterns. Because estrogen levels are highest during proestrus and cholinergic facilitation appears to be limited to this time, it is suggested that estrogen priming of central cholinergic systems is necessary for the cholinergic regulation of sexual behavior in intact, cycling female rats.

Animals↗
PubMedDate not supplied

Short and long term inhibitory actions of alpha-melanocyte stimulating hormone on lordosis in rats.

The effects of 200 ng of intracerebroventricularly (ICV) and 20 micrograms of subcutaneously (SC) administered alpha-melanocyte stimulating hormone (MSH) on lordosis in rats were examined. Previous research, employing crossover designs, has revealed significant effects of MSH on lordosis. The results of Experiments 1a and 1b suggest that similar designs produce significant effects even in the absence of MSH. Thus, it is not clear that previous results were due exclusively to an action of MSH. Experiment 2 employed a modification of previous procedures and indicated that MSH administered either SC or ICV inhibited receptivity in subjects displaying high levels of responding. Moreover, MSH administered SC was also found to facilitate receptivity in subjects displaying low levels of responding. However, a possible long term inhibitory action of MSH on receptivity was also revealed. Because animals were tested repeatedly, this brought into question the results of Experiment 2. Procedures were revised accordingly and the effects of MSH re-examined. The results of Experiment 3 indicated that MSH administered SC facilitated receptivity while MSH administered ICV inhibited receptivity. In addition, MSH administered ICV exerted an inhibitory effect one week after administration. Therefore, MSH appears to exert both short and long-acting effects on sexual receptivity.

Animals↗
PubMed1996

Influence of opioid peptides on the priming action of estrogen on lordosis in ovariectomized rats.

Lordosis in response to male mounting in estrogen-progesterone primed ovariectomized rats was facilitated by beta-endorphin or metenkephalin but inhibited by leu-enkephalin if the peptides were injected into third ventricle at the time of estrogen-priming. It is suggested that opioidergic systems modulate the activation of the estrogen-dependent brain functions that control lordosis.

Animals↗
PubMedDate not supplied

Alterations by estrogen and hypothyroidism in the effects of septal lesions on lordosis behavior of male rats.

Earlier experiments indicated that chronic exposure to estradiol benzoate (EB) following septal lesions can increase the subsequent levels of female sexual behavior in male rats tested several months later following priming doses of EB. However, the present study demonstrates that a single injection of a large dose of EB (50 microng) two days after septal destruction did not modify subsequent responsiveness to EB priming in male rats relative to sham operated controls. Yet male rats given 10 daily injections of 5.0 microng EB/day immediately following a septal lesion were more responsive to EB than oil treated controls when tested later for lordosis behavior. Therefore, the capacity for EB to alter the behavioral effects of septal lesions on lordosis behavior in male rats is related to both chronic administration and a period of susceptibility to some action of EB during the immediate post-lesion period. In two additional experiments, chronic hypothyroidism induced by propylthiouracil or thyroidectomy was also found to modify the effects of septal lesions on female sexual behavior of male rats. These latter results indicate that EB is not unique in its capacity to alter the behavioral effects of septal lesions in male rats, and are consistent with the view that both EB and hypothyroidism may interact with some dynamic process associated with recovery from brain lesions.

Animals↗
PubMedDate not supplied

Effects of septal lesions and chronic estrogen treatment on dopamine, GABA and lordosis behavior in male rats.

Septal lesions (SL) in female rats result in an increased sensitivity to the behavioral effects of acute estradiol benzoate (ACUTE-EB; 2 microgram/day X 3) treatment as measured by the lordosis quotient (LQ: number of lordotic responses X 100/number of mounts). Male rats, intact or castrated, do not show this enhanced behavioral response to ACUTE-EB unless they are treated with EB (2 microgram/day) for 2--4 weeks immediately following the production of SL. The present study was undertaken to examine possible neurochemical alterations which could account for the enhanced behavioral sensitivity to ACUTE-EB seen in the SL male rat treated chronically with EB during the postlesion period (SL-EB). Three groups, normal males, SL-EB and SL males chronically treated with oil (SL-oil), were subdivided and treated with ACUTE-EB or oil and decapitated. The brains were removed, frozen and stored at -50 degrees C prior to dissection and assay. Tyrosine hydroxylase (TH) activity was assayed in the dopamine (DA) rich areas of the forebrain (striatum, STR, nucleus accumbens septi, ACB; and olfactory tubercle). The TH activity was significantly suppressed in both the STR and ACB of the SL-EB males treated with ACUTE-EB. The glutamic acid decarboxylase (GAD) activity in both the substantia nigra and ventral tegmentum was significantly increased in the SL-EB males given ACUTE-EB relative to that of all other groups. In summary, SL-EB males given ACUTE-EB show (1) an enhanced LQ, (2) decreased TH activity in the region of DA terminals, and (3) increased GAD activity in the region of DA cell bodies. The increase in GAD activity is suggested to be a result of an altered neuronal feedback because of plastic changes that occur during chronic EB treatment following production of SL. This probable increase in inhibitory tone in the region of the DA cell bodies may explain the observation that the SL-EB male exhibits decreased DA turnover following ACUTE-EB treatment. Moreover, since DA may be inhibitory to the display of lordosis behavior, the SL-EB males may show an enhanced LQ, at least partially, because of this reduction in DA activity.

Animals↗
PubMedDate not supplied

Reduced ovarian function and lordosis behavior following hypothalamic knife cuts.

Lordosis behavior (LQ) estrous cycles and ovarian status were studied in the same animals following either frontal (FC), frontolateral (FLC) or sham (S) surgical interruption of medial basal hypothalamic (MBH) neural connections made with a modified Halász knife (1.5 mm radius). LQ was studied in adult female rats at 7, 30, 105 and 180 day after FC, FLC or S and estrous cycles were monitored for 28 day after cuts. Vaginal cytology examined before and after S surgery indicated regular 4-5 day cycles, whereas after FC vaginal cytology became predominately cornified and after FLC it was variable. Ovarian weights and appearance at ovariectomy (OVX) supported cycle data: S ovaries had recent corpora lutea (CL); FC gonads were smaller with no recent CL and FLC gonads appeared atrophic. Multiple regression analysis of individual FC and FLC dimensions indicated that cut location and dimensions contributed significantly to the length of postoperative estrus periods. After OVX all animals were tested for LQ after estradiol benzoate (EB) and EB plus progesterone (P) priming. Although there were no group LQ differences after EB alone, S and FC animals showed an increase in LQ after EB plus P, whereas, FLC rats showed no change and this effect persisted for 180 day. Multiple regression analysis of FC and FLC coordinates indicated that the more posterior and lateral extending cuts were associated with lower LQ scores. Collectively, these data suggest a role for similar anterolateral MBH neural connections in (1) basal and cyclic gonadotrophin release and (2) EB plus P effects on lordosis behavior.

Animals↗
PubMedDate not supplied

Disruption of lordosis by dorsal midbrain lesions in the golden hamster.

Bilateral lesions of the dorsal midbrain at levels from the anterior to posterior deep tectum abolished lordosis responses to males or manual stimuli. The lesions also blocked reflexive head turning and biting responses to tactile stimulation of the face. Unilateral dorsal midbrain lesions impaired responses to stimuli impinging upon the contralateral body and/or face without affecting lordosis responses to ipsilaterally-applied manual stimuli. The pattern of deficits following unilateral lesions was consistent with the known somatosensory organization of the dorsal midbrain, but the uniform effectiveness of the bilateral lesions placed at any anterior-posterior level of the dorsal midbrain may have been due to bilateral interruption of central gray efferents in addition to deep tectal neuronal damage. Neither bilateral nor unilateral lesions had to involve the central gray to produce their effects.

Animals↗
PubMed1991

Ibotenic acid-induced lesions of the medial zona incerta decrease lordosis behavior in the female rat.

To examine the role of the medial zona incerta (mZI) in female sexual behavior, ovariectomized estrogen- and progesterone-treated female rats were tested for sexual receptivity after bilateral injections of the selective neurotoxin ibotenic acid (3 micrograms/0.3 microliter) directly into the mZI. These injections produced a significant attenuation of lordosis behavior in highly receptive females when compared with saline-injected controls. This decrease in sexual receptivity was also reflected in a significant increase of rejections of male mount attempts. However, these lesions did not abolish the display of lordosis behavior. In addition, the frequency of hopping and darting was decreased in ibotenic acid-injected females when compared with controls. Consistent with previous studies, these lesions also produced a transient impairment of drinking behavior (hypodipsia) typical of rats with large electrolytic lesions of the mZI. This study demonstrates that mZI neurons play a role in mediating sexual receptivity in the female rat. Collectively, these results suggest that in addition to the projection from the ventromedial nucleus of the hypothalamus to the midbrain central gray, the functional integrity of the mZI is of crucial importance for the expression of sexual receptivity in the female rat.

Animals↗
PubMed2006

Rats bred for high versus low anxiety responses neonatally demonstrate increases in lordosis, pacing behavior, and midbrain 3 alpha, 5 alpha-THP levels as adults.

Duration and intensity of lordosis is mediated by actions of the progesterone (P) metabolite, 3 alpha-hydroxy-5 alpha-pregnan-20-one (3 alpha,5 alpha-THP) at GABA-sub(A) receptors in the midbrain ventral tegmental area. Because rats selectively bred for infantile vocalizations may differ in endogenous 3 alpha,5 alpha-THP secretion, their sexual behavior, midbrain, and plasma 3 alpha,5 alpha-THP levels as adult rats in behavioral estrus was examined. Rats bred for high rates of infantile vocalizations had shorter latencies and intervals between intromissions and ejaculation, higher lordosis quotients and ratings, more pacing of their sexual contacts, and had higher P and 3 alpha,5 alpha-THP levels in plasma and midbrain than did rats bred for low rats of infantile vocalizations. Thus, levels of 3 alpha,5 alpha-THP in the midbrain are associated with differences in sexual behavior of these rats.

Animals↗
PubMed1983

beta-Endorphin regulates lordosis in female rats by modulating LH-RH release.

Several lines of evidence have implicated the endogenous opioid peptides in the regulation of masculine sexual behaviour. However, although the opioid related peptides alpha-melanocyte stimulating hormone (alpha-MSH) and adrenocorticotropin (ACTH) have been shown to affect lordosis behaviour in the female rat, there is as yet no evidence for a role of the endogenous opiates in the regulation of female sexual behaviour. We present here evidence that the endogenous opiates in the mesencephalic central grey (MCG) are involved in the control of lordosis behaviour in the female rat.

Animals↗
PubMed1997

Progesterone receptor participates in the stimulatory effect of LHRH, prostaglandin E2, and cyclic AMP on lordosis and proceptive behaviours in rats.

We explored the effect of the antiprogestin RU486 on the estrous behaviour (lordosis and proceptivity) induced in sexually experienced ovariectomized oestrogen primed rats by: 5 microg luteinizing hormone-releasing hormone (LHRH), 100 microg prostaglandin E2 (PGE2), or 2 mg dibutyryl cyclic AMP (db cAMP). Pretreatment with 5 mg RU 486 (but not with vehicle) 60 min before the injection of the above-mentioned agents significantly decreased both lordosis and proceptive behaviours normally induced by such agents. Results suggest that the estrus-inducing action of LHRH, PGE2 and db cAMP occurs through the activation of the progesterone receptor.

Animals↗
PubMed2001

Ventral tegmental area infusions of inhibitors of the biosynthesis and metabolism of 3alpha,5alpha-THP attenuate lordosis of hormone-primed and behavioural oestrous rats and hamsters.

The importance of progesterone biosynthesis and metabolism to 5alpha-pregnan-3alpha-ol-20-one (3alpha,5alpha-THP), which exerts its effects via GABAA/benzodiazepine receptor complexes (GBRs) rather than intracellular progestin receptors (PRs), was investigated for its effects on sexual receptivity. Epostane, a 3beta-hydroxysteroid dehydrogenase inhibitor, blocks progesterone and 3alpha,5alpha-THP biosynthesis. Finasteride, a 5alpha-reductase inhibitor, blocks the metabolism of progesterone to dihydroprogesterone (DHP), which is subsequently metabolized to 3alpha,5alpha-THP. Indomethacin, a 3alpha-hydroxysteroid oxidoreductase inhibitor, blocks DHP's metabolism to 3alpha,5alpha-THP, and its oxidation to DHP. Epostane, finasteride, indomethacin or vehicle were infused intracranially in the ventral tegmental area (VTA) of hormone-primed or naturally receptive rats and hamsters and sexual behaviour was recorded. Epostane, finasteride and indomethacin to the VTA significantly reduced lordosis, compared to vehicle infusions, in hormone-primed and behavioural oestrous rats and hamsters. Radioimmunoassay revealed that concentrations of midbrain 3alpha,5alpha-THP were reduced following epostane, finasteride or indomethacin infusions that significantly decreased lordosis. Immunocytochemistry for 3alpha,5alpha-THP revealed the number of immunoreactive cells were significantly reduced in the VTA following epostane, finasteride or indomethacin infusion to the VTA, but not other midbrain sites. These data suggest that biosynthesis of progestins, and the metabolism of progesterone to 3alpha,5alpha-THP in the VTA, are important for progestin-facilitated sexual receptivity of rats and hamsters.

Androstenols↗
PubMed2006

The vomeronasal organ is required for the expression of lordosis behaviour, but not sex discrimination in female mice.

The role of the vomeronasal organ (VNO) in mediating neuroendocrine responses in female mice is well known; however, whether the VNO is equally important for sex discrimination is more controversial as evidence exists for a role of the main olfactory system in mate recognition. Therefore, we studied the effect of VNO removal (VNOx) on the ability of female mice to discriminate between volatile and non-volatile odours of conspecifics of the two sexes and in different endocrine states using Y-maze tests. VNOx female mice were able to reliably distinguish between male and female or male and gonadectomized (gdx) male volatile odours. However, when subjects had to discriminate between male and female or gdx male non-volatile odours, VNOx females were no longer able to discriminate between sex or different endocrine status. These results thus show that the VNO is primarily involved in the detection and processing of non-volatile odours, and that female mice can use volatile odours detected and processed by the main olfactory system for mate recognition. However, VNO inputs are needed to promote contact with the male, including facilitation of lordosis responses to his mounts. A single subcutaneous injection with gonadotropin-releasing hormone (GnRH) partially reversed the deficit in lordosis behaviour observed in VNOx females suggesting that VNO inputs may reach hypothalamic GnRH neurons to influence the display of sexual behaviour.

Analysis of Variance↗