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PubMed1988

Transmitter and peptide actions on hypothalamic neurons in vitro: implications for lordosis.

This article summarizes a series of studies using brain tissue slices of rats to record single-unit activity from the hypothalamic ventromedial nucleus (VMN) and preoptic area (POA), both of which are crucial for the regulation of the estrogen-dependent feminine mating behavior, lordosis. In these studies the actions of acetylcholine (ACh), serotonin (5HT), norepinephrine (NE), luteinizing hormone-releasing hormone (LHRH), arginine-vasopressin (AVP), and oxytocin (OXY) on neuronal activity were investigated. The results show that these agents could evoke either direct responses or neuromodulatory changes from VMN or POA cells in vitro. Comparison of the net neuronal actions of each of these agents with their effects on lordosis behavior revealed interesting correlations. All the excitatory agents, i.e., ACh, AVP, OXY, and LHRH, have been indicated by intracerebral application studies to be facilitatory on lordosis. The inhibitory agent, 5HT, could inhibit lordosis, when applied to the VMN and its vicinity. Such correlations indicate that these transmitters and peptides can facilitate or inhibit lordosis by increasing or decreasing, respectively, the frequency of action potentials in the types of hypothalamic neurons recorded here.

Action Potentials↗
PubMed2004

Estrogen and progesterone dose-dependently reduce disruptive effects of restraint on lordosis behavior.

Ovariectomized rats were hormonally primed with various doses of estradiol benzoate (EB; 0.5-10 microg) in combination with various doses of progesterone (2.5-500 microg) to induce sexual receptivity. Females were then subjected to 5 min restraint and the effect on lordosis behavior was monitored for the next 30 min. Such mild stress has been previously shown to transiently reduce lordosis behavior of ovariectomized females hormonally primed only with 10 microg EB. In the current study, doses of progesterone of 25 microg or more in combination with 10 microg EB reduced the effects of restraint. Also priming doses of EB from 4.0 to 10 microg in combination with 250 microg progesterone prevented the lordosis-inhibiting effects of restraint. These findings reinforce prior observations of the dose-dependency of both estrogen and progesterone in the facilitation of lordosis behavior and introduce the female's lordosis response to mild restraint as a potentially useful index of the female's response to stress.

Animals↗
PubMed2006

Progestin facilitation of lordosis in rodents involves adenylyl cyclase activity in the ventral tegmental area.

Increasing cAMP, or activating dopamine type 1 (D(1)) or GABA(A)/benzodiazepine receptor complexes (GBRs), in the ventral tegmental area (VTA) enhances lordosis of rodents. Whether D(1)- and/or GBR-mediated increases in progestin-facilitated lordosis involve the cAMP-synthesizing enzyme, adenylyl cyclase, in the VTA, was investigated. In Experiment 1, ovariectomized estradiol (E(2); 10 microg at h 0)+progesterone (P; 250 microg at h 45)-primed hamsters first received bilateral infusions of the adenylyl cyclase inhibitor, 2',5'-dideoxyadenosine (DDA; 12 microM/side), or vehicle, and then were infused with the D(1) agonist, SKF38393 (100 ng/side), the GBR agonist, muscimol (100 ng/side), or vehicle, to the VTA. Lordosis was evaluated before and 30 min after each infusion. In Experiment 2, ovariectomized, E(2)-primed (10 microg at h 0) rats received VTA infusions of DDA (12 microM/side) or vehicle; SKF38393 (100 ng/side), muscimol (100 ng/side), or vehicle; and the neurosteroid, 5alpha-pregnan-3alpha-ol-20-one (3alpha,5alpha-THP; 100 or 200 ng/side), or beta-cyclodextrin vehicle. Lordosis was assessed before the series of infusions, immediately after drug infusions and 10 or 60 min after 3alpha,5alpha-THP infusions. Progestin- or progestin plus SKF38393-or muscimol-mediated increases in lordosis were blocked by DDA pretreatment. Thus, in the VTA, progestins' membrane action may involve adenylyl cyclase.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2006

In the ventral tegmental area, progestins have actions at D1 receptors for lordosis of hamsters and rats that involve GABA A receptors.

In the ventral tegmental area (VTA), progestins facilitate lordosis via actions at gamma-aminobutyric acid (GABA)(A)/benzodiazepine receptor complexes (GBRs) and dopamine type 1 receptors (D1). The relationship between progestins' actions at GBRs and D1 in the VTA for facilitating sexual behavior of hamsters and rats was examined. Ovariectomized (ovx), estradiol (E(2); 10 microg)+progesterone (P; 250 microg; SC)-primed hamsters, with bilateral guide cannulae to the VTA, were pre-tested for sexual and motor behavior and infused with the GBR antagonist bicuculline (100 ng/side) or vehicle. Thirty minutes later, hamsters were re-tested and then infused with the D1 agonist SKF38393 (100 ng/side) or vehicle. Hamsters were post-tested 30 min later. Ovx, E(2) (10 microg)-primed rats were pre-tested, infused first with bicuculline or vehicle, second with SKF38393 or vehicle, third with 5alpha-pregnan-3alpha-ol-20-one (3alpha,5alpha-THP; 0, 100, or 200 ng) and were post-tested 10 and 60 min after 3alpha,5alpha-THP infusions. VTA infusions of SKF38393 increased lordosis of hamsters or rats. Bicuculline pretreatment reduced SKF38393- and/or progesterone-mediated increases in lordosis of E2-primed hamsters. In E2-primed rats, bicuculline blocked SKF38393- and/or 3alpha,5alpha-THP-mediated increases in lordosis. There were no effects on motor behavior. Thus, in the VTA, GBR activity modulates D1-mediated actions for lordosis of hamsters and rats.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1998

Lordosis-enhancing medial preoptic area lesions do not alter hypothalamic estrogen receptor- or progestin receptor-immunoreactivity in prepubertal female guinea pigs.

Female guinea pigs rarely display adult-typical lordosis responses to ovarian steroid hormones until 40-50 days of age. Behavioral hyporesponsiveness in prepubertal females may be due, in part, to deficiencies in hypothalamic estrogen receptors and/or estradiol-induced progestin receptors. This study was designed to test the hypothesis that bilateral medial preoptic area (MPOA) lesions, which enhance the display of progesterone-facilitated lordosis in juvenile females, increase levels of hypothalamic estrogen receptors and/or estradiol-induced progestin receptors. Hartley guinea pigs were ovariectomized at 11-12 days of age and at 14-15 days of age received bilateral electrolytic or sham lesions aimed at the MPOA. At approximately 3 weeks of age, lesioned and sham-lesioned animals were either tested for the display of progesterone-facilitated lordosis or perfused, and their hypothalamic tissue processed for estrogen receptor- or estradiol-induced progestin receptor-immunostaining. Although a significantly higher percentage of MPOA-lesioned than sham-lesioned guinea pigs displayed progesterone-facilitated lordosis (85.7% vs. 5. 8%, respectively, p<0.05), there were no significant lesion-related differences in the number or staining intensity of cells containing estrogen receptor- or estradiol-induced progestin receptor-immunoreactivity in the ventrolateral hypothalamus or arcuate nucleus. These data do not support the hypothesis that the enhanced display of progesterone-facilitated lordosis in prepubertal guinea pigs following MPOA lesions is due to increased hypothalamic concentrations of estrogen receptors or estradiol-induced progestin receptors.

Animals↗
PubMed2002

Olanzapine and progesterone have dose-dependent and additive effects to enhance lordosis and progestin concentrations of rats.

There is evidence that actions of both progesterone (P) and its metabolite, 5alpha-pregnane-3alpha-ol-20-one (3alpha,5alpha-THP), are important for sexual behavior of estradiol (E(2))-primed rodents. Olanzapine, an atypical antipsychotic, dose-dependently increases 3alpha,5alpha-THP in the cortex of male rats. These experiments investigated the effects of olanzapine administration on female sexual behavior and progestin concentrations. In Experiment 1, ovariectomized (ovx) rats (N=128) were primed with estradiol benzoate (EB) at Hour 0 and were administered P (0, 50, 100, or 200 microg sc) at Hour 44 and olanzapine (0.0, 2.5, 5.0, or 10.0 mg/kg ip) at Hour 47. At Hour 48, rats were tested for sexual receptivity with a stimulus male. Administration of 10.0 mg/kg of olanzapine, irrespective of P, significantly increased the occurrence (lordosis quotients, LQs) and the intensity (lordosis ratings, LRs) of lordosis compared to all other dosages. Administration of 2.5 or 5.0 mg/kg of olanzapine, irrespective of P, increased LQs and LRs compared to vehicle administration. Olanzapine without P dose-dependently increased LQs and LRs. As expected, administration of P without olanzapine also dose-dependently increased LQs and LRs. In Experiment 2, ovx rats (N=44, n=4 per group) received EB (0 or 10 microg sc), P (0 or 200 microg sc), and/or olanzapine (0.0, 2.5, 5.0, or 10.0 mg/kg ip). The same pattern of effects seen for lordosis was observed on progestin concentrations. Whole brain and plasma P and 3alpha,5alpha-THP concentrations were increased with olanzapine or P dosing and were greatest with coadministration. Together, these data demonstrate that olanzapine and P have independent effects to increase lordosis, P, and 3alpha,5alpha-THP concentrations of adult rats and additive effects in combination, suggesting complimentary mechanisms of action.

Animals↗
PubMed1983

GnRH in the spinal subarachnoid space potentiates lordosis behavior in the female rat.

Gonadotropin releasing hormone (GnRH) (100 ng) infused directly into the spinal subarachnoid space via a chronically implanted catheter, induced a prompt facilitation of lordosis behavior in estrogen-primed ovariectomized female rats. Facilitation occurred within 5 min and lasted for 3 1/2 hr. This effect of GnRH could be blocked by a GnRH antagonist analog, [D-Phe2, Pro3, D-Phe6] GnRH (250 ng) which also completely abolished lordosis within 2 1/2 hr. The antagonist analog (250 ng) but not a high titre specific anti-GnRH antiserum (enough to neutralize 24 micrograms of GnRH) abolished lordosis when infused alone in the subarachnoid space in estrogen-primed rats. The antagonist but not the anti-GnRH antiserum also significantly suppressed lordosis in estrogen-progesterone primed female rats. Supporting experiments showed that the effects of GnRH and its antagonist may not be due to their effects on supraspinal structures by diffusion from the spinal subarachnoid space. These results may indicate a direct effect of GnRH and its antagonist at the level of the spinal cord and may suggest a possible role for GnRH in the processing of somatosensory information necessary for the trigger of lordosis.

Animals↗
PubMed1987

Brain transections differentially alter lordosis and ear wiggling of 6-day-old rats.

Six-day-old male and female rats display lordosis and ear wiggling in response to tactile stimulation of the flanks and rump, without priming by exogenous estrogen. The involvement of various brain regions in these behaviors, which resemble components of adult female sexual behavior, was examined by making acute transections along the neuraxis from the olfactory tract to the medulla in 6-day-old rats. Four to 5 hr after the transection procedure, pups were tested for lordosis and ear wiggling. Lordosis was severely reduced or eliminated in pups with cuts through the hindbrain or diencephalon (above the level of the mammillary bodies) but was relatively unaffected by cuts through the posterior hypothalamus and rostral tegmentum and by cuts rostral to the anterior hypothalamus. Ear wiggling was disrupted by transections throughout the hindbrain and was facilitated only in females by transections throughout the forebrain (anterior to the mammillary bodies). These data suggest that facilitation from the hypothalamus is required for lordosis in the infant rat and the forebrain inhibitory systems for ear wiggling are functional in female infants by 6 days of age. Similarities and differences between the neural control of lordosis and ear wiggling in infant and adult rats suggest that the infant sex-like behaviors may be precursors of adult female sexual behavior.

Animals↗
PubMed1998

Time course of VMN lesion effects on lordosis and ultrasound production in hamsters.

Lesions of the ventromedial hypothalamus (VMN) depress lordosis but increase ultrasonic vocalization in female hamsters. These changes are consistent with the behavioral incompatibility of lordosis and ultrasound production and suggest that the VMN coordinates short-term changes in these behaviors. In keeping with past results, unilateral lesions disrupted lordosis responses to contralateral flank stimulation. The change appeared within 15 min after the lesion and was much more rapid than the corresponding effect in rats. For hamsters, these findings support other evidence suggesting VMN mediation of somatosensory, not just hormonal, influences on lordosis. In a companion study, ultrasound rates became depressed within 15 min of bilateral lesion of the VMN, suggesting a role for the VMN in the short-term control of ultrasound production. Calling at later time intervals was facilitated by the lesions. The direction and time course of the lesion effects on lordosis and ultrasound production suggest that the VMN cannot easily account for the behavioral incompatibility of these 2 responses.

Analysis of Variance↗
PubMed1985

Differential effects of lesions in three limbic areas on ultrasound production and lordosis by female hamsters.

Ultrasound production and lordosis were examined in ovariectomized, hormone-primed female hamsters before and after sham operations or bilateral electrolytic lesions in the lateral septum/bed nucleus, corticomedial amygdala, or lateral habenula. During 2-min exposures to synthetic ultrasounds and 1-min exposures to stimulus males, females with corticomedial amygdala lesions exhibited reduced ultrasound rates and lordosis durations. Following lesions in the lateral septum/bed nucleus, females showed significant increases in ultrasound rates with no pre- to postoperative change in lordosis. Ablations of the lateral habenula had no effect on calling but were associated with shorter lordosis durations. These results demonstrate that two reproductive behaviors, ultrasound production and lordosis, are differentially affected, depending on lesion placement within the limbic system. In turn, these differences demonstrate that the neural mechanisms for two elements of a single major class of behavior can be quite distinct, both in terms of the likelihood that particular brain areas will be involved and in the nature of their involvement.

Amygdala↗
PubMed1981

Inhibition of lordosis in rats by the antiestrogen CI-628 in the absence of progesterone.

A series of experiments assessed whether the ability of the antiestrogen CI-628 to inhibit estrogen-stimulated lordosis in adult ovariectomized rats depends upon its interference with the synergistic effects of estrogen with progesterone. In Experiment 1, the effect of CI-628 was contrasted in rats brought into estrus by a single subcutaneous injection of estradiol benzoate (EB) combined with an injection of progesterone (P) 42 hr later versus four daily injections of EB (without any P). CI-628 was given at the time of EB injection(s). CI-628 substantially and equally effectively antagonized lordotic responding in both conditions. In the absence of CI-628, rats receiving progesterone had significantly higher lordosis scores than the 4-day EB control animals. In Experiment 2, rats receiving CI-628 on only the first 2 of 4 days of EB injections had significantly decreased lordosis scores unless P was also given on the day of testing. This suggested that the EB from the latter injections was not acting as a progestin "mimic." In Experiment 3, lordotic responding stimulated by EB (without P) was inhibited by CI-628 in rats that were both ovariectomized and adrenalectomized. This suggested that adrenal progestins were not involved in the ability of CI-628 to inhibit lordosis. Taken together, the results suggest that the mechanism of action of CI-628 for the inhibition of lordosis does not depend upon its ability to antagonize an estrogen-induced increase in neural progestin receptors. Implications of this for estrogen-mediated behaviors, for which CI-628 has little or no antagonistic effects, are discussed.

Animals↗
PubMedDate not supplied

Correlation of back extensor strength with thoracic kyphosis and lumbar lordosis in estrogen-deficient women.

Aging and osteoporosis have been associated with skeletal changes. Back extensor strengthening exercises are highly recommended for management of back pain, especially back pain related to osteoporosis. To our knowledge, the correlation of thoracic kyphosis, lumbar lordosis, and sacral inclination with back extensor strength, physical activity, and bone mineral density has not been critically studied in healthy, active, estrogen-deficient women. In a study of 65 such women (ages 48-65 yr), back extensor strength, bone mineral density, and physical activity score were evaluated and measured. These factors were then correlated with radiographic factors: (1) vertebral body ratios (anterior/posterior height) calculated for each vertebra from T-4 through L-5; (2) kyphosis index determined by adding the anterior heights of each vertebral body, T-4 through T-12, and then dividing the total by the corresponding sum of the posterior heights of each vertebral body; (3) thoracic kyphosis; (4) lumbar lordosis; and (5) sacral inclination. Back extensor strength had a significant negative correlation with thoracic kyphosis (r = -0.30, P = 0.019) and a positive correlation with lumbar lordosis (r = 0.26, P = 0.048) and sacral inclination (r = 0.34, P = 0.009). However, bone mineral density and physical activity score did not show any significant correlations with the radiographic factors. The results indicate that the stronger the back extensor, the smaller the thoracic kyphosis and the larger the lumbar lordosis and sacral inclination. We conclude that back extensor strength is an important determinant of posture in healthy women. However, prescribing back extensor strengthening exercises alone may also increase lumbar lordosis, which is not desirable.

Aged↗
PubMed1979

Intrahypothalamic implants of progesterone inhibit lordosis behavior in ovariectomized, estrogen-treated rats.

Intracranial implants of crystalline progesterone (P) were used to examine in site of action of P's facilitatory and inhibitory effects on lordosis behavior in the ovariectomized, estradiol-benzoate (EB)-primed RAT. P implanted in the medial basal hypothalamus (MBH) 1 h prior to subcutaneous (s.c.) EB injection inhibited lordosis in response to a systemic P injection 44 h after EB (concurrent inhibition). P implanted in the MBH did not facilitate lordosis when implanted 44 h after EB injection, but this same implant of P inhibited lordosis in response to P injection 68 h after EB (sequential inhibition). Cholesterol (Chol) implants in the MBH did not inhibit lordosis behavior in either the concurrent or the sequential inhibition experimental paradigms. The results indicate that the MBH is an important site of P inhibition of sexual receptivity in the rat.

Animals↗
PubMed1982

Inhibition of lordosis behavior by intrahypothalamic implants of pargyline.

Hypothalamic sites responsible for monoaminergic of gonadal hormone-facilitated female sexual behavior (the lordosis response) were investigated. Pargyline, an irreversible inhibitor of monoamine oxidase, was applied stereotaxically to the hypothalamus of ovariectomized, estrogen-primed females 2 h prior to progesterone administration. Application of pargyline dorsal to or within the lateral aspect of the ventromedial nucleus led to a reduction in lordosis quotients and quality scores 5-7 and 29-31 h later. Implantation dorsal to or within the dorsomedial nucleus did not inhibit lordosis responding 5-7 h later but did inhibit the response 29-31 h later. In both implant sites, lordosis responding returned to prepargyline levels within 55 h after drug placement. The effects of the pargyline cannulae were verified biochemically by measuring activity of monoamine oxidase in preoptic-hypothalamic nuclei. Enzyme activity was inhibited to some extent in all nuclei sampled. The ability of the implants to antagonize lordosis responding was related to the extent to which they inhibited monoamine oxidase activity in the hypothalamus. Results suggest that localized perturbations in hypothalamic cells whose monoamine metabolism is known to be affected by gonadal hormones is sufficient to affect female sexual behavior.

Animals↗
PubMed1983

Modulation of the lordosis reflex of female rats by LHRH, its antiserum and analogs in the mesencephalic central gray.

Effects of intracerebral infusion of LHRH and related compounds on the lordosis reflex were examined in ovariectomized, estrogen-treated female rats. Lordosis, triggered either by manual cutaneous stimulation or by male mounting, was facilitated by the infusion of LHRH dissolved in saline into the mesencephalic central gray at midcollicular levels (CG). Infusion of an anti-LHRH globulin into the CG disrupted lordosis. Pretreatment with estrogen was necessary to obtain the behavioral facilitation by LHRH infusion. In separate experiments, placement of cannulae containing LHRH in an agar-saline gel in the CG also facilitated lordosis behavior. LHRH analogs applied to the CG by this method showed a clear dissociation between their behavioral effects and their reported effects on LH release. Cellular mechanisms involved in the mediation of LHRH effect in midbrain for the facilitation of lordosis may be different from those in gonadotrophs for LH release.

Animals↗
PubMed1996

Inhibitory effect of baclofen on lordosis in female and male rats with dorsal raphe nucleus lesion or septal cut.

The inhibitory effect of baclofen, a GABAB receptor agonist, on lordosis was examined in female and male rats with dorsal raphe nucleus lesions (DRL) or cut of the septal fibers (ARD). Both female and male DRL and ARD rats showed higher lordosis quotients (LQ) than corresponding controls without brain surgery. This indicates that the dorsal raphe nucleus and the septum exert lordosis-inhibiting influences in female and male rats. After treatment with 10 mg/kg baclofen, the mean LQs in female control and female ARD groups were significantly lower than those of vehicle-treated control and ARD females. In DRL females, however, LQs did not decrease, even after the injection of baclofen. In males, baclofen also diminished lordosis in ARD rats, but not in DRL rats. These results suggest that the GABAB receptor system plays an inhibitory role in regulating lordosis behavior not only in female but also in male rats. Furthermore, the function of the GABA neurons depends on the inhibitory mechanism of the dorsal raphe nucleus in the regulation of female sexual behavior.

Animals↗
PubMed2006

Microgravity-induced modifications of the vestibuloocular reflex in Xenopus laevis tadpoles are related to development and the occurrence of tail lordosis.

UNLABELLED: During space flights, tadpoles of the clawed toad Xenopus laevis occasionally develop upward bended tails (tail lordosis). The tail lordosis disappears after re-entry to 1g within a couple of days. The mechanisms responsible for the induction of the tail lordosis are unknown; physical conditions such as weight de-loading or physiological factors such as decreased vestibular activity in microgravity might contribute. Microgravity (microg) also exerts significant effects on the roll-induced vestibuloocular reflex (rVOR). The rVOR was used to clarify whether tail lordosis is caused by physiological factors, by correlating the occurrence of microg-induced tail lordosis with the extent of microg-induced rVOR modifications. Post-flight recordings from three space flights (D-2 Spacelab mission, STS-55 in 1993; Shuttle-to-Mir mission SMM-06, STS-84 in 1997; French Soyuz taxi flight Andromède to ISS in 2001) were analyzed in these experiments. At onset of microgravity, tadpoles were at stages 25-28, 33-36 or 45. Parameters tested were rVOR gain (ratio between the angular eye movement and the lateral 30 degrees roll) and rVOR amplitude (maximal angular postural change of the eyes during a 360 degrees lateral roll). A ratio of 22-84% of tadpoles developed lordotic tails, depending on the space flight. The overall observation was that the rVOR of tadpoles with normal tails was either not affected by microgravity, or it was enhanced. In contrast, the rVOR of lordotic animals always revealed a depression. In particular, during post-flight days 1-11, tadpoles with lordotic tails from all three groups (25-28, 33-36 and 45) showed a lower rVOR gain and amplitude than the 1g-controls. The rVOR gain and amplitude of tadpoles from the groups 25-28 and 33-36 that developed normal tails was not affected by microgravity while the rVOR of microg-tadpoles from the stage-45 group with normal tails revealed a significant rVOR augmentation. IN CONCLUSION: (1) the vestibular system of tadpoles with lordotic tails is developmentally retarded by microgravity; (2) after a critical status of vestibular maturation obtained during the appearance of first swimming, microgravity activates an adaptation mechanism that causes a sensitization of the vestibular system.

Animals↗
PubMed2002

Decrease of serotonin and metabolite in the forebrain and facilitation of lordosis by dorsal raphe nucleus lesions in male rats.

In castrated male rats, a radiofrequency lesion was made in the dorsal raphe nucleus (DRL) and lordosis behavior was observed following treatment with estrogen. After the behavioral test, brains were removed and the contents of 5-HT and 5-HIAA in the forebrain were measured by high pressure liquid chromatography (HPLC). In the results, only 2 of 16 control males without brain surgery showed lordosis, and the mean lordosis quotient (LQ) was extremely low when compared to that in control females. In contrast, all male rats with DRL displayed lordosis and the mean LQ was higher than that of control males without brain surgery but lower than that in control females (P < 0.001). In the DRL males, 5-HT and 5-HIAA contents in the septum (SPT), the preoptic area (POA), the ventromedial hypothalamus (VMH) and the striatum (STM) were lower than those in control male and female groups (P < 0.001). These results suggest that the dorsal raphe nucleus prevents male rats from showing lordosis by serotonergic influence in the forebrain. In addition, HPLC results showed that levels of the 5-HT in the SPT, the POA and the VMH in the female group were higher than those in the control male group (P < 0.05). In female rats, the POA (P < 0.01) and the VMH (P < 0.05) contained larger 5-HT than those in the SPT and the STM, but there were no difference of 5-HT contents in the male rat.

Animals↗