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PubMed1975

Lordosis behavior and mounting behavior in male rats: effects of castration and treatment with estradiol benzoate or testosterone propionate.

Male rats were selected for showing or not showing lordosis in response to manual stimulation. They were subsequently tested for mounting behavior with receptive females and for lordosis behavior in response to manual stimulation and to male mounting. Males showing lordosis as intacts displayed this behavior more readily following castration or castration and treatment with estradiol benzoate or testosterone propionate than males which did not show lordosis before castration. No group differences in mounting behavior could be detected under any of the endocrine conditions studied. It is suggested that the neural mechanisms mediated mounting and lordosis are dissociated and that individual differences in the occurrence of lordosis in male rats are due to differences in neural sensitivity to estrogen.

Animals↗
PubMed1985

Hormonal control of the perception of the olfactory signals which facilitate lordosis behavior in the male rat.

This study was designed to evaluate in the male rat the hormonal requirements for the facilitation of feminine behavior by the odor of male urine. Wistar rats from the WI and WII strains in our colony were orchidectomized (ORCH) as adults. A first group was given a single dose of 75 micrograms estradiol benzoate (EB) and tested for lordosis behavior 48 hr later. Exposure to the odor of male urine by 9 +/- 1 hr before the behavioral session did not increase the number of animals showing lordosis behavior as compared to non exposed controls. A second group of WI rats was given 0.5 micrograms EB every day for 4 to 8 days. A similar number of animals displayed lordosis behavior irrespective of whether they were exposed to the odor of urine before testing. A third group of WI rats was injected with 75 micrograms EB and 1 mg progesterone (P) 39 hr apart. Exposure to the odor of urine during estrogen treatment remained ineffective but significantly increased the number of animals showing lordosis behavior when performed at the time of P injection. A last group of WII rats was given 25 micrograms EB and 100 micrograms or 150 micrograms P 39 hr apart. Although uncapable as such to facilitate lordosis behavior the dose of 100 micrograms P rendered the animals responsive to the odor of urine. It was concluded that (1) the perception by feminized males of olfactory signals from the male was dependent on P; (2) an interaction between hormonal and sensory mechanisms was involved in the facilitation of lordosis behavior in the male rat.

Animals↗
PubMed1987

Effects of ventromedial nucleus lesions on the display of lordosis behavior in the male rat. Interactions with facilitory effects of male urine.

Previous observations showed that exposure to the odor of male urine prior to mating could enhance the display of lordosis behavior in male rats feminized with ovarian hormones. This study was performed to determine in feminized male rats whether the control of lordosis behavior by the olfactory system was mediated by the ventromedial nucleus (VMN) of the hypothalamus. Male rats were orchidectomized (ORCH) as adults and primed with 25 micrograms estradiol benzoate (EB) and 150 micrograms progesterone (P) 40 hr apart. Lordosis behavior was tested 9 +/- 1 hr after P injection. VMN lesions were shown to completely suppress the display of lordosis behavior as compared to sham VMN operated and dorsomedial nucleus (DMN) lesioned animals. Exposure of feminized rats to the odor of male urine by 9 +/- 1 hr before mating significantly increased the proportion of ORCH rats that displayed lordosis behavior in response to male mounts. This effect was abolished by VMN lesions but was maintained in the sham VMN operated and DMN lesioned animals. These results were discussed in the light of the present knowledge on the neuroendocrine and olfactory structures which mediate lordosis behavior in the male rat.

Animals↗
PubMed1988

Effects of cholecystokinin on male copulatory behavior and lordosis behavior in male rats.

Because the distribution of cholecystokinin octapeptide (CCK-8) within the hypothalamus and limbic system overlaps with steroid concentrating regions, and because these areas are involved in the regulation of reproductive behaviors, we examined the effects of exogenous CCK-8 on male copulatory behavior and lordosis behavior in the male rat. Peripheral administration of a dose of CCK-8 that altered lordosis behavior in females (3 micrograms/kg, intraperitoneal) was ineffective in altering male copulatory behavior in males, either before or after gonadectomy, and was also ineffective in altering lordosis behavior after estrogen priming. In a separate experiment, CCK-8 injected into the lateral ventricle also did not affect male copulatory behavior, but lordosis behavior was increased dramatically after gonadectomy and estrogen priming. Although these results do not answer the question whether CCK-8 is acting to inhibit a neural system that normally suppresses lordosis behavior or is acting to stimulate a facilitatory circuit, these results do indicate the existence of an estrogen sensitive neural substrate in males on which CCK can act to facilitate lordosis behavior.

Amygdala↗
PubMed1989

Lordosis inhibiting effects of endogenous progesterone in the male rat primed with estrogen.

The aim of this study was to investigate the mechanisms involved in the inhibitory action of progesterone on estrogen-induced facilitatory effects of estradiol benzoate on lordosis behavior in the male rat. Intact adult male rats were given 1) 25 micrograms estradiol benzoate (EB) and 100 micrograms progesterone (P) at an interval of 42 hr. EB injected animals served as controls 2) EB followed by 3 doses of 400 micrograms dexamethasone (DEXA) and P as above. EB + DEXA injected animals served as controls. Testing for lordosis behavior was performed by 50 +/- hr after EB injection. A significant decrease in the number of the males displaying lordosis in response to the mounts of stimulus males resulted from P injection following EB treatment as compared to EB controls. DEXA treatment significantly reduced the number of EB animals showing lordosis responses but completely prevented the inhibitory effects of exogenous P to occur. Blood P values appeared to be significantly lower in EB + DEXA males than in their EB counterparts. The results provide evidence that endogenous P is involved in the display of lordosis behavior by EB-treated intact males. They mainly suggest that the effects of exogenous P on estrogen-induced lordosis behavior in the intact male rat result from sequential inhibitory mechanisms involving exposure of the animals to the successive action of endogenous and exogenous P.

Animals↗
PubMed1990

Changes in hypothalamic neuronal function related to hormonal induction of lordosis in behaving hamsters.

The hypothalamus is known to be critical for the neuroendocrine control of sexual behavior, but the neural effects of gonadal hormones on behavior-related activity of hypothalamic neurons has received little investigation. The present study examined the effects on single hypothalamic neurons of lordosis-inducing estrogen and progesterone administration to behaving golden hamsters. The lordosis-inducing action of the hormones was associated with rapidly emerging, cumulative changes in the activity level and somatosensory responsiveness of neurons throughout the hypothalamus, as well as the appearance in most neurons of lordosis-correlated firing. This functional reconfiguration of hypothalamic neuronal properties resembled, in time course and other aspects, effects of estrogen and progesterone previously observed in hamster midbrain neurons. Although the firing rates of the hypothalamic neurons were typically low, the lordosis-related activity of these neurons was compatible with a role in the control of individual episodes of lordosis as well as a state-related tendency to exhibit the lordosis response.

Animals↗
PubMed1993

Cuts between the septum and preoptic area increase ultrasound production, lordosis, and body weight in female hamsters.

Studies of the mechanisms for female-typical mating behavior have focused on the ventromedial hypothalamus, and on the decrements in lordosis caused by lesions of this structure. However, opposed changes of comparable size are produced, at least in rats, by horizontal cuts extending forward from the anterior commissure (anterior roof deafferentation, or ARD). This suggests the existence of a lordosis-inhibiting system of forebrain structures that may include the lateral septum and preoptic area. To test the generality of this system, ovariectomized hamsters in hormone-induced estrus were observed for levels of ultrasound production and lordosis during tests with male conspecifics. In addition, subjects were observed for lordosis responses to light manual stimulation. Upon the completion of these tests, subjects received control treatments or ARD prior to a second round of behavioral observations. These postoperative tests revealed clear ARD-stimulated increases in ultrasound production and body weight. In contrast, the facilitation of lordosis was more subtle, appearing in tests with manual stimulation, but not in response to males. These results, then, demonstrate some consistency across species in the effects of ARD. At the same time, however, they suggest species differences in the magnitude of these effects, in turn, suggesting species differences in the dependence of receptivity on forebrain lordosis-inhibiting mechanisms.

Afferent Pathways↗
PubMed1994

The effects of intraventricular injection of beta-endorphin on initial estrogen action to induce lordosis behavior.

Ovariectomized female rats subcutaneously (SC) injected or intracerebrally implanted with estradiol benzoate (EB), and given progesterone SC were used as experimental animals to assess the effects of the beta-endorphin (beta-EP) neuronal system on lordosis behavior. In intraventricular (IV) injection of beta-EP at the onset of sc EB priming, the lordosis behavior was significantly (p < 0.001) facilitated. In contrast, the lordosis behavior was significantly (p < 0.001) inhibited by IV injection of naloxone, an opioid receptor antagonist. beta-EP facilitation of lordosis was observed exclusively within the initial stage of estrogen action. The behavior was significantly (p < 0.001) facilitated by IV injection of beta-EP given with an intracerebral implantation of crystalline EB into the septal-preoptic regions. However, the lordosis behavior was significantly (p < 0.001) inhibited by beta-EP when EB was implanted into the ventromedial hypothalamus. Animals receiving EB implants into the mesencephalic reticular formation were not affected by beta-EP. The present study suggests that the beta-EP neuronal system stimulates sexual receptivity through an action on the central nervous system in relation to the site of estrogen-initial activation to induce the lordosis reflex. The sites of beta-EP action may be the estrogen receptive septal-preoptic and hypothalamic regions; the former for facilitatory effect and the latter for inhibitory effect.

Animals↗
PubMed1986

Reversible disruption of lordosis via midbrain infusions of procaine and tetrodotoxin.

Behavioral effects of bilateral intracranial infusions of tetrodotoxin (1, 3.3 or 10 ng/rat), 50% procaine (2 microliters/rat) or phosphate-buffered saline (PBS-2 microliters/rat) into the dorsal midbrain of conscious, lightly-restrained female rats were evaluated. High levels of lordotic responsiveness were induced in ovariectomized animals treated with estradiol (E2) capsules or subcutaneous injections of estradiol benzoate (EB) followed by progesterone (P). The effect of each of the 3 infusates on lordosis was determined using manual stimulation and lordosis quotient determinations. In addition, the vocalization by an animal during lordosis measurements, paw withdrawal to pinch, righting reflex latency and recognition of a platform edge were also monitored. Within 2 minutes following procaine or tetrodotoxin (TTX) infusions in E2 implanted rats, lordotic responsiveness declined sharply. Whereas procaine-treated animals returned to control levels of responsiveness within 20 minutes, TTX infusions induced a more prolonged depression of lordosis lasting up to 8 hours. Infusions of PBS had no effect on any of the behaviors. In a separate group of animals treated with either E2 or EB + P and infused with 10 ng TTX the time course of the decline in lordotic responsiveness was identical for both steroid treatments. Paw withdrawal was unaffected by TTX while all other measured behaviors were disrupted along the same time course as lordosis. Collectively the above results implicate the requirement of sodium-dependent neuronal activity within dorsal midbrain for the maintenance of the lordosis reflex, along with other behavioral responses influenced by this brain region.

Animals↗
PubMed1987

Separation of dopaminergic and serotonergic inhibitory mechanisms in the mediation of estrogen-induced lordosis behaviour in the rat.

The administration of the putative 5-hydroxytryptamine1 (5-HT1) agonist 8-hydroxy-2(di-n-propylamino) tetralin (8-OH-DPAT) (0.0625-1.0 mg X kg-1) suppresses lordosis behaviour induced in ovariectomized female rats by daily treatment for 3-5 days with estradiol benzoate (1.25 micrograms/rat). A similar suppressive effect on the lordosis behaviour can be obtained by administration of the dopamine/serotonin agonist, lisuride (0.1-0.4 mg X kg-1), or after the administration of the dopamine (DA) agonists, apomorphine (0.2-0.8 mg X kg-1) or quinpirole (0.75-2.50 mg X kg-1). The suppressive effects on the lordosis behaviour by 8-OH-DPAT cannot be antagonized by the DA receptor antagonist haloperidol (0.2 mg X kg-1) neither with methiotepin (0.5 mg X kg-1), which is assumed to be a non-selective 5-HT receptor blocking agent, nor with pirenperone (0.25 mg X kg-1) which is assumed to be a 5-HT2 receptor blocking agent. However, a partial blockade of the lordosis suppressive effects of 8-OH-DPAT was obtained by treatment with (-)-pindolol, which is thought to be a partial 5-HT1 blocking agent, suggesting that 8-OH-DPAT exerts its suppressive effects on the lordosis behaviour through the 5-HT system. Haloperidol causes a complete blockade of the suppressive effects of apomorphine and quinpirole suggesting that these drugs exert their inhibitory effects on the lordosis behaviour by activating the DA system.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1988

Lordosis facilitation in estrogen primed rats by intrabrain injection of pregnanes.

Progesterone (P) and nine of its natural metabolites were bilaterally injected (5 micrograms in 0.5 microliter oil) into either the ventromedial hypothalamus (VMH) or the medial preoptic area (MPOA) of estrogen primed rats to assess their relative potencies for stimulating lordosis. P, 5 alpha-pregnanedione and 5 beta, 3 beta-pregnanolone elicited lordosis when injected at either VMH or MPOA. By contrast, 5 alpha, 3 beta-pregnanolone as well as 20 alpha-OH and 20 beta-OH-pregnenone were much more effective in stimulating lordosis when implanted in the MPOA. Finally, 5 beta-pregnanedione and 5 beta,3 alpha-pregnanolone did not stimulate lordosis at neither VMH nor MPOA. The observation that lordosis was induced in estrogen primed rats both by pregnanes that bind to the P receptor (i.e., P; 5 alpha-pregnanedione; 20 alpha- and 20 beta-OH-pregnenone) and by pregnanes that do not (i.e., 5 alpha, 3 beta-; 5 beta,3 beta- and 5 alpha,3 alpha-pregnanolone) indicates that diverse cellular mechanisms are involved in the facilitation of lordosis by pregnanes.

Animals↗
PubMed1986

Acute effects of sex steroids on lordosis behaviour of the female rat.

In the present series of experiments, dose-response and time-response relationships between single injections of sex steroids and the display of lordosis behaviour in the female rat, were investigated. When injected 48 h prior to testing, increasing doses of estradiol benzoate (EB) or testosterone propionate (TP) resulted in increasing levels of lordosis behaviour. TP was much less effective than EB in facilitating lordosis behaviour in the female rat. The optimum time interval between hormonal treatment and testing was 48-72 h for TP, but 48 h for EB. Single injections of dihydrotestosterone propionate (DHTP), also injected 48 h prior to testing, inhibited lordosis behaviour in EB-primed female rats. DHTP-inhibition of lordosis behaviour in EB-primed female rats was most effective when given prior to and least effective when given after EB-treatment. Progesterone, injected 4 h prior to testing, facilitated lordosis in EB-, TP- or EB + DHTP-treated female rats.

Animals↗
PubMedDate not supplied

Lesions of the preoptic area facilitate lordosis behavior in male and female guinea pigs.

Male and female guinea pigs received radiofrequency lesions in the medial preoptic area (MPOA). Animals were gonadectomized, treated with estrogen and progesterone, and tested for the occurrence of the lordosis response to manual stimulation. Females with MPOA lesions exhibited enhanced lordosis behavior, shorter latencies to heat, longer duration of heat and longer maximum lordosis duration than sham control females. In males with MPOA lesions, the lordosis response could be elicited by manual stimulation, in contrast to no response in the sham control males. Furthermore, MPOA-lesioned males were insensitive to the inhibitory effects of progesterone on lordosis behavior, while MPOA-lesioned females were as sensitive as sham controls to the inhibitory effects of progesterone. The results suggest that a neural mechanism resides within the MPOA which inhibits the occurrence of lordosis behavior in both male and female guinea pigs and which is not involved in a sexual dimorphism in responsiveness to progesterone.

Animals↗
PubMed1986

Lordosis-disrupting tectal lesions alter midbrain unit somatosensory responsiveness in hamsters.

Previous research has shown that bilateral deep tectal lesions in golden hamsters abolish the lordosis response, whereas unilateral lesions selectively impair lordosis elicitation by contralateral flank stimulation. The present study analyzed the neural basis of these lesion effects by assessing the somatosensory responsiveness of midbrain neurons in three groups of urethane-anesthetized hamsters: animals with lordosis-abolishing bilateral tectal lesions, animals with lordosis-impairing unilateral lesions, and intact animals. Animals with bilateral lesions differed from the other groups in three aspects of unit sensory responsiveness by showing: (1) the highest percentage of neurons responsive to somatic stimulation, (2) the highest incidence of unit responsiveness to flank stimulation, and (3) the greatest proportion of responsive neurons in the ventral tegmentum. Hamsters with unilateral lesions showed basically normal unit responsiveness apart from elevated unit response to face stimulation. The results suggest that bilateral tectal lesions may eliminate lordosis by the combined effects of enhanced ventral tegmental somatosensory responsiveness and tectal destruction. Unilateral lesions appear to impair lordosis without changing the somatosensory excitability of remaining midbrain neurons.

Animals↗
PubMed1989

Patterns of 2-deoxyglucose uptake reflect the neural processing of lordosis-inducing somatosensory stimuli in hamsters.

Semi-quantitative [14C]2-deoxyglucose (2DG) autoradiography was used to map the neural responses of female hamsters to lordosis-inducing flank stimuli. Specifically, manual stimulation of one flank was used to maintain estrous females in lordosis for 20 min after an IV injection of 200 muCi/kg of 2DG. Hemispheric differences in 2DG uptake then were sought in brain nuclei implicated in the programming of lordosis, or in the mediation of somatosensory or hormonal influences on this response. The responses to lateralized flank stimulation included reliable contralateral elevations in 2DG uptake in the ventral posterior lateral nucleus of the thalamus (VPL), the dorsal mesencephalic central gray (dCG), and the tectum. Elevated activity on the part of the VPL may not be crucial for lordosis. However, the effects of flank stimulation on 2DG uptake by the dCG and tectum confirm and extend much previous evidence implicating the dorsal midbrain in the mediation of tactile and hormonal effects on sexual responses. For example, these results suggest that somatosensory influences on hamster lordosis are mediated by both the dCG and tectum. In addition, they suggest that these influences are strongly lateralized until at least this stage of sensory processing, leaving for some subsequent element of neural circuitry the task of translating these lateralized inputs into the bilaterally symmetric outputs ultimately required to program the normal, bilaterally symmetric, lordosis response.

Animals↗
PubMed1993

Functional relationships between mesencephalic central gray and septum in regulating lordosis in female rats: effect of dual lesions.

In order to clarify the functional relationships between the lateral septum (LS) and the mesencephalic central gray (MCG) in regulating lordosis behavior, ovariectomized female rats received dual lesions in these two areas. In the first experiment, females with unilateral (right or left, R-MCGL or L-MCGL) or bilateral MCG (B-MCG) lesions were subjected to behavioral tests after the implantation of a Silastic tube containing estradiol. Lordosis was observed in only one B-MCGL female. In the R-MCGL and L-MCGL groups, most females displayed lordosis, but lordosis quotients (LQ) were significantly lower than that of the control group. These results suggest the importance of the MCG in lordosis regulation, and that there is no functional laterality in the MCG. In the second experiment, B-MCGL or R-MCGL females received bilateral LS lesions (LSL). The lordotic activity in the LSL + B-MCGL group was extremely low, being comparable to that of B-MCGL alone. On the other hand, in the LSL + R-MCGL females, the LQ was significantly higher than that of females with R-MCGL alone and was comparable to that of controls. Thus, the lateral septum plays an inhibitory role in regulating lordosis, but the influence of the lateral septum is not stronger than the facilitatory influence of the mesencephalic central gray, because the LSL could not recover the suppressive effect of the MCGL.

Animals↗
PubMed2002

GABAergic drugs alter hypothalamic serotonin release and lordosis in estrogen-primed rats.

The effects of muscimol, a GABA(A) agonist, and phaclofen, a GABA(B) antagonist, on serotonin (5HT) release in the mediobasal hypothalamus and lordosis behavior were studied in freely moving rats using in vivo microdialysis. Two days after implantation of bilateral guide cannulae directed towards the ventromedial nucleus of the hypothalamus (VMH), ovariectomized rats were primed with estradiol (E(2)). The rats were implanted with microdialysis probes 24 h later. Following a pretest for lordosis, perfusate 5HT was measured at 20-min intervals until the baseline was stable. The rats were treated with 10, 30 or 100 microM muscimol or 30 and 100 microM phaclofen in artificial CSF delivered via reverse dialysis for 40 min. Control animals were continuously perfused with artificial CSF. Behavior was tested 20, 60 and 180 min after introduction of the drug. Decreased hypothalamic 5HT (40-60% of baseline) and marked facilitation of lordosis were present 20 min after administration of either drug. The effects of 10 and 30 microM muscimol and 30 microM phaclofen on both 5HT and lordosis were reversed after 180 min. Reversal of the behavioral and neurochemical effects were not evident in either the 100 microM muscimol or 100 microM phaclofen groups at the time-points tested. Proceptive responses were observed in phaclofen-treated rats but not in rats treated with muscimol. Levels of hypothalamic 5HT and lordosis quotients in control rats did not significantly differ from initial values. These results suggest that GABAergic effects on lordosis may be mediated through an interaction with 5HT in the mediobasal hypothalamus.

Animals↗
PubMed2003

Progesterone attenuates the effect of the 5-HT1A receptor agonist, 8-OH-DPAT, and of mild restraint on lordosis behavior.

Ovariectomized, hormone-primed rats were used to test the hypothesis that progesterone treatment attenuated the effects of the 5-HT(1A) receptor agonist, (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), on female rat lordosis behavior. Based upon prior evidence that prepriming with estradiol benzoate (EB) reduced the ability of 8-OH-DPAT to inhibit lordosis behavior, rats were preprimed with 10 microg EB 7 days before a second priming with 10 microg EB followed 48 h later with 500 microg progesterone or vehicle. Independent of the presence of progesterone, prepriming with EB attenuated the lordosis-inhibiting effects of systemic treatment with 8-OH-DPAT. However, progesterone also reduced the effects of 8-OH-DPAT and this effect was also seen in females primed only once with EB. In contrast, progesterone was relatively ineffective in attenuating the effects of bilateral infusion with 8-OH-DPAT into the ventromedial nucleus of the hypothalamus (VMN). The failure of progesterone to substantially reduce the effects of VMN infusion with 8-OH-DPAT contrasts with prior studies in which estrogen's protective action against the drug did include the VMN. Thus, while both estrogen and progesterone reduce the lordosis-inhibiting effect of 8-OH-DPAT, the mechanisms responsible for the effects of the two gonadal hormones may be different. Priming with progesterone also prevented the effects of 5 min of restraint. When rats were hormonally primed with EB and oil, rats showed a transient, but significant, decline in lordosis behavior 5 and 10 min after restraint. Rats primed with EB and progesterone were unaffected by the restraint. These results are discussed in terms of their implications for the role of progesterone in altering the 5-HT(1A) receptor modulation of lordosis behavior.

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