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PubMed1997

Infusion of CCK-A receptor mRNA antisense oligodeoxynucleotides inhibits lordosis behavior.

Cholecystokinin (CCK) acting on discrete receptors in the limbic-hypothalamic circuit modulates lordosis behavior. Neurons in the medial preoptic nucleus (MPN) express CCK-A subtype receptor mRNA, and site-specific infusions of CCK facilitate lordosis, suggesting that CCK-A receptor activation positively modulates lordosis. In the present study, we demonstrated CCK binding in the central portion of the MPN (MPNc) and the disruption of lordosis behavior by reducing the expression of CCK-A receptors in this nucleus. Antisense oligodeoxynucleotides (ODN) specific for CCK-A receptor mRNA were infused into the MPN of ovariectomized female rats. The expression of estrogen-induced lordosis behavior was blocked in animals receiving infusions of antisense ODN into the MPN (LQ = 10.0 +/- 1.0) compared to animals receiving infusions of nonsense ODN (containing the same nucleotide bases in a random order; LQ = 92.5 +/- 7.5). In vitro, AR42J pancreatic acinar carcinoma cells treated with antisense ODN had lower levels of CCK-A and CCK-B subtype receptor binding than nonsense ODN treated cells. In vivo, however, infusions of CCK-A mRNA antisense ODN did not alter CCK-B receptor binding levels. These results suggest that CCK, acting via CCK-A receptors in the MPNc, is critical for the display of lordosis behavior.

Animals↗
PubMed1998

Mapping of neural and signal transduction pathways for lordosis in the search for estrogen actions on the central nervous system.

Estrogen can act on the brain to regulate various biological functions and behavior. In attempts to elucidate the estrogen action, the rodent female reproductive behavior, lordosis, was used as a model. Lordosis is an estrogen-dependent reflexive behavior and, hence, is mediated by discrete neural pathways that are modulated by estrogen. Therefore, a strategy of mapping the pathways, both neural and biochemical, and examining them for estrogen effect was used to localize and subsequently analyze the central action of estrogen. Using various experimental approaches, an 'inverted Y-shaped' neural pathway both sufficient and essential for mediating lordosis was defined. The top portion is a descending pathway conveying the permissive estrogen influence which originated from hypothalamic ventromedial nucleus relayed via midbrain periaqueductal grey down to medullary reticular formation, the top of the spino-bulbo-spinal reflex arc at the bottom. This estrogen influence alters the input-output relationship, shifting the output toward more excitation. With this shift in output, estrogen can enable the otherwise ineffective lordosis-triggering sensory stimuli to elicit lordosis. In the ventromedial nucleus, the origin of the estrogen influence, a multidisciplinary approach was used to map intracellular signaling pathways. A phosphoinositide pathway involving a specific G protein and the activation of protein kinase C was found to be involved in the mediation of lordosis as well as a probable target of the permissive estrogen action. The action of estrogen on this signal transduction pathway, a potentiation, is consistent with and, hence, may be an underlying mechanism for the estrogen influenced shift toward excitation. Thus, further investigation on this specific signal transduction pathway should be helpful in elucidating the action of estrogen on the brain.

Animals↗
PubMed1975

Vaginal stimulation in rats induces prolonged lordosis responsiveness and sexual receptivity.

Sexual receptivity to males resulted from stimulation of the vagina with a glass rod in previously unreceptive ovariectomized, estrogen-treated rats. Several minutes of rejection behavior preceded the receptivity. In a second study, manual palpation was used to determine the duration of the lordosis response facilitation. Initially, all females were unresponsive to manual flank-perineum stimulation (palpation). Vaginal stimulation plus palpation, which together elicit lordosis, facilitated subsequent lordosis responses to palpation. This effect persisted for several hours after the vaginal stimulation was applied. Vaginal stimulation alone, which was ineffective in eliciting lordosis, also facilitated lordosis in response to subsequent palpation. Repeated palpation did not facilitate lordosis. These prolonged effects were independent of hormone treatment.

Animals↗
PubMed1976

Lordosis in the male golden hamster elicited by manual stimulation: characteristics and hormonal sensitivity.

The lordosis response was regularly elicited from 24 of 31 intact, adult male hamsters, using manual somatosensory stimulation of the dorsal rear body. In these males there was no correlation between measures of male-typical behavior and lordosis. Castration had no effect on male lordosis duration scores even when intromissions were eliminated. Combined treatment with estradiol benzoate and progesterone significantly increased male lordosis duration scores. The body surface was mapped with a standardized brush stimulus. For eliciting lordosis, effectiveness of stimulation increased in an almost identical manner for hormone-primed males and females from the anterior to the posterior part of the body, with the stimulation of flanks, rump, and perineum the most effective. Within each skin zone, absolute effectiveness was greater in females than in males. Various types of somato-sensory stimulation were compared for their effectiveness in eliciting lordosis. Females were more responsive to these stimuli than males, even when males were hormonally primed. These behavioral data have implications for concepts of the neural organization of male- and female-typical mating responses existing within the same individual.

Animals↗
PubMed1980

LH-RH in the mesencephalic central grey can potentiate lordosis reflex of female rats.

The lordosis reflex, which characterises female reproductive behaviour in rodents, can be potentiated in oestrogen-primed ovariectomised female rats by electrical stimulation of the ventromedial nucleus of the hypothalamus (VMN). Subsequent demonstration of an immediate and large facilitation of the lordosis reflex from the mesencephalic central grey (CG) prompted us to speculate that the VMN may exert an oestrogen-dependent tonic bias on the mesencephalic circuitry for lordosis via its heavy descending projections. Moreover, we considered that luteinising hormone-releasing hormone (LH-RH) could be involved in this system. LH-RH can potentiate lordosis when given systemically to oestrogen-primed ovariectomised rats, and neurotropic effects of this peptide have been shown by microiontophoresis. Also, some axons in the CG have been stained with antiserum to LH-RH. The present study examined a possible role of LH-RH in the CG in the regulation of the lordosis reflex of oestrogen-primed ovariectomised female rats. Infusion of exogenous LH-RH in the CG had an immediate facilitative effect on the lordosis reflex, whereas passive immunisation against endogenous LH-RH by anti-LH-RH gamma-globulin diminished the reflex.

Animals↗
PubMed1999

Cyclic GMP may potentiate lordosis behaviour by progesterone receptor activation.

The purpose of this study was to test the hypothesis that cGMP acts as a progesterone substitute to facilitate lordosis in oestrogen-primed rats. Female Sprague-Dawley rats underwent stereotaxic surgery to place a 26-gauge guide cannula into the third ventricle. Bilateral ovariectomy was done at the same time as stereotaxic surgery. Five days later ovariectomized rats were primed with 2 microg estradiol benzoate 24 and 48 h prior to behaviour testing. Some animals were further injected with 200 microg progesterone 4 h before behaviour testing. A nitric oxide synthase inhibitor infused into the third ventricle before progesterone administration significantly reduced lordosis performance. 8-Bromo-cGMP, a cell permeable cGMP analogue, or saline vehicle was infused into the third ventricle of hormone-primed animals approximately 4 h prior to the first of 3-h behaviour tests. This cGMP analogue facilitated lordosis behaviour. We next used KT5823, a highly specific inhibitor of protein kinase G (PKG), to test the hypothesis that cGMP action is mediated by this kinase. In this experiment, KT5823 was infused 15 min before progesterone. KT5823 significantly decreased lordosis behaviour. RU486, a progesterone receptor antagonist, was used to assess whether the stimulatory effects of cGMP are mediated through the progesterone receptor. Oestrogen-primed animals were injected with 5 mg of RU486 or vehicle 60 min before infusion with 8-bromo-cGMP. RU486 significantly attenuated cGMP-facilitated lordosis behaviour. These data show that cGMP facilitates lordosis through activation of PKG and the progesterone receptor.

Alkaloids↗
PubMed1999

Progestins' rapid facilitation of lordosis when applied to the ventral tegmentum corresponds to efficacy at enhancing GABA(A)receptor activity.

Progestins may have actions in the midbrain though gamma-aminobutyric acid (GABA)A/benzodiazepine receptor complexes (GBRs) that are relevant for sexual receptivity. The efficacy and time course of various progestins to enhance lordosis when applied to the ventral tegmental area (VTA), following progesterone to the ventral medial hypothalamus (VMH) was investigated. Ovariectomized, oestrogen-primed rats and hamsters with contralateral VMH/VTA cannulae were tested for lordosis before and after implants of P to the VMH and progestins to the VTA. The progestins were P, 5alpha-pregnan-3,20-dione (DHP), 5alpha-pregnan-3alpha-ol-20-one(3alpha,5alpha-TH P), 5alpha-pregnan-3alpha,21-diol-20-one (THDOC), 5beta-pregnan-3alpha-ol-20-one(3alpha,5beta-THP) , 17alpha-ol-6-methyl-4,6-pregnadiene-3,20-dione-17-acetate (megestrol acetate, MA), and 6-chloro-17-ol-4,6-pregnadiene-3, 20-dione-17-acetate (chlormadinone acetate, CA). Progestins' effects on GABA-mediated chloride influx and SR 95531 binding in cortical and midbrain tissue, respectively, were examined in rats and hamsters. 3alpha,5alpha-THP and THDOC implants to the VTA were the most effective at immediately facilitating lordosis of rats and hamsters. Two hours later all other progestins, except MA and CA, increased lordosis in rats; only P, 3alpha,5alpha-THP, and THDOC were effective in hamsters. The progestins' effectiveness at facilitating lordosis were similar to their effects on GABA-stimulated chloride influx and SR 95531 receptor binding (3alpha,5alpha-THP and THDOC>P>DHP>3alpha, 5beta-THP>MA and CA). These findings suggest that progesterone lordosis enhancing effects in the rodent VTA may be via GBRs.

Animals↗
PubMed1999

Maintaining lumbar lordosis with anterior single solid-rod instrumentation in thoracolumbar and lumbar adolescent idiopathic scoliosis.

STUDY DESIGN: A prospective radiographic evaluation of 20 consecutive patients with primary lumbar or thoracolumbar adolescent idiopathic scoliosis who were treated with anterior convex compressive single solid-rod spinal instrumentation and structural titanium mesh (Harms) cages. OBJECTIVES: To evaluate a lordosis-preserving anterior single solid-rod instrumented fusion technique for these specific adolescent idiopathic curves. SUMMARY OF BACKGROUND DATA: Maintaining instrumented segmental lumbar lordosis after anterior fusion and instrumentation for thoracolumbar and lumbar curves has been difficult. Twenty consecutive patients who underwent anterior single solid-rod fusion, aged 18 or younger with a primary thoracolumbar or lumbar curve, were observed for preservation of lordosis for a minimum of 2 years. METHODS: All patients underwent an identical anterior surgical technique, involving discectomies and anulectomies of all convex discs, structural titanium mesh (Harms) cages placed in the anterior half of all disc spaces below T12, morselized rib autograft packed in all disc spaces to be fused and inside the cages, and anterior single solid-rod (5.0-mm or 5.5-mm diameter) convex compressive spinal instrumentation with appropriate lordotic rod contour and rod rotation as necessary. The anterior rod was placed just posterior to the cages to optimize lordotic contouring of the spine during compression. None of the patients was braced after surgery. The lowest instrumented vertebrae (LIV) were L2 (n = 3), L3 (n = 15), and L4 (n = 2), typically the lower end vertebra of the Cobb measurement. RESULTS: Measurements for the primary coronal Cobb before surgery, 1 week after surgery, and 2 years after surgery were 48 degrees, 11 degrees, and 12 degrees; for C7 plumb line deviation from the midline: 3.6 cm, 1.9 cm, and 1.2 cm; for lowest instrumented vertebra translation: 31 mm, 15 mm, and 15 mm; and for LIV tilt: 29 degrees, 6 degrees and 6 degrees, respectively. Sagittal measurements before surgery, 1 week after surgery, and 2 years after surgery were: T12-L2: -1 degree, -6 degrees, and -6 degrees; T12-LIV: -8 degrees, -13 degrees, -9 degrees; T12-S1: -61 degrees, -56 degrees, -60 degrees; and entire instrumented levels: -6 degrees, -9 degrees, and -6 degrees, respectively. Coronal plane correction improved: 75% in the primary Cobb, 66% in the plumb line, 50% in LIV translation, and 80% in LIV tilt. Sagittal plane alignment improved in T12-L2 lordosis (P < 0.01) with preservation of physiologic lordosis in the instrumented levels, T12-LIV, and T12-sacrum. There were no instrumentation failures, pseudarthroses, or reoperations. CONCLUSIONS: Coronal plane correction with preservation of thoracolumbar and lumbar lordosis 2 years after anterior convex compressive spinal instrumentation was accomplished using a lordotically contoured single solid rod with structural cages placed anteriorly in the disc spaces of patients with primary thoracolumbar or lumbar adolescent idiopathic scoliosis.

Adolescent↗
PubMed1982

Cycle of lordosis behavior in female hamsters whose circadian activity rhythm has split into two components.

Within 75 days of exposure to constant light (LL), the circadian activity rhythm of 21 of 32 hamsters had dissociated or "split" into two distinct components. These components were labeled either evening (E) or morning (M) depending on whether they appeared to be derived from the E or M portion of the activity phase prior to the occurrence of "splitting." Both regular (i.e., 4-day) and irregular (i.e., non-4-day) cycles in lordosis behavior were observed in all of the animals with an intact activity rhythm and in 18 of the 21 animals with a split rhythm of activity. The onset of behavioral estrus always occurred near the time of the onset of locomotor activity in animals with an intact activity rhythm. Among the females with a split activity rhythm, seven showed lordosis onsets only near the onset of the E component whereas five others began lordosis behavior only near the onset of the M component. Importantly, in five animals the onset of lordosis was associated on different days with either the E or M component. These results indicate that cycles in lordosis behavior persist even after the circadian rhythm of activity has dissociated into two components, and that at least one component of the estrous cycle, onset of lordosis behavior, can be coupled to either of two oscillators that underlie the circadian rhythm of locomotor activity in hamsters.

Animals↗
PubMed1979

Triggering of lordosis reflex in female rats with somatosensory stimulation: quantitative determination of stimulus parameters.

1. Pressure on the skin of the tail base and perineum of female rats in the range of 40--440 millibars, following bilateral contact with the flanks, was adequate to elicit the lordosis reflex. Hair deflection alone or noxious stimulation was neither sufficient nor necessary for lordosis behavior to occur. 2. For a given pressure, increasing the area of stimulation increased the effectiveness for evoking lordosis; inputs from mechanoreceptors at different skin locations can be summated to trigger the behavioral response. 3. During mating behavior, increased pressure from the male rat on the skin of the female, in the range of 50--450 millibars, was associated with increased probability and strength of lordosis. 4. Increasing the dose of estrogen increased the probability of lordosis to a given pressure stimulus. The hormone effect can be characterized as a facilitation of the throughput from low-threshold pressure receptors on tail base and perineum to motoneurons for the lumbar vertebral dorsiflexion of lordosis.

Animals↗
PubMed1984

Joint and separate effects of estrogen and progesterone on responses of midbrain neurons to lordosis-controlling somatic stimuli in the female golden Syrian hamster.

Single midbrain neurons were examined for effects of ovarian hormone administration on responsiveness to an array of lordosis-controlling types of somatosensory stimuli in anesthetized, ovariectomized Syrian hamsters. Neuronal responses were recorded under four different hormonal treatment conditions: 1) estradiol benzoate (EB) followed by progesterone (P), 2) EB alone, 3) P alone, or 4) no hormone administration. Only the hamsters receiving both EB and P showed lordosis in a mating test immediately prior to preparation for recording. The joint administration of EB and P strongly facilitated unit responsiveness to lordosis-eliciting (e.g., lumbosacral tactile) forms of stimulation. The incidence of units showing sustained changes in firing of at least +/- 30% in response to these stimuli was highest in animals having received EB and P (69%) and lowest in those given P alone (37%), with the occurrence of responsive units significantly different across the four hormonal conditions. The magnitude of the median unit response to lordosis-trigger stimuli in hamsters given EB and P was significantly higher than unit responses in hamsters receiving either P alone or no hormone. Bilateral shoulders stimulation, a weak stimulus for lordosis elicitation, produced the most responses in units from animals given EB and P (42%) and the fewest in hamsters given EB alone (12%), with a significant difference in responsiveness across the hormonal conditions. The incidence of units responding exclusively to facial stimulation, which is strongly antagonistic to lordosis in behaving animals, was greatest in hamsters injected with P alone (22%) and least for cells from the animals given both EB and P (6%). The difference in unit responsiveness to this stimulus across the four hormone conditions was significant. Analysis of unit-response patterns by the multivariate technique of discriminant analysis revealed that neuronal responses to most stimuli, especially flanks, back, shoulders, and face, were differentially affected by the hormone treatments such that these response patterns could be used to identify the four hormonal conditions from which the neurons were sampled. In addition, the hormonal treatments were found to have influenced the incidence of accelerative or decelerative unit responses to somatic stimuli. Discriminant analysis of unit responses as a function of location of the cells within the midbrain showed that neurons in the tectum and central gray had response patterns highly distinguishable from each other as well as from those of cells in the central and ventromedial tegmental regions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Hypothalamic serotonin lesions unmask hormone responsiveness of lordosis behavior in adult male rats.

Hypothalamic lesions of serotoninergic afferents following bilateral stereotoxic injections of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) into the region of the ventromedial hypothalamus enhanced the effects of hormonally induced lordosis responding in both male and female rats. However, similarities and differences in the enhanced responsiveness to ovarian hormones were observed between the sexes. Compared with sham-lesioned controls, lesioned males displayed elevated lordosis responding to estradiol (E) priming alone, as well as to priming with E followed by progresterone (P). On the other hand, lesioned females displayed elevated lordosis in response to E priming alone, but were not different from controls in a synergistic facilitation of lordosis by P after E priming. With respect to receptivity, neither lesioned nor control males displayed ear-wiggling and hop-darting in response to E + P, whereas both lesioned and control females were proceptive following this treatment. Therefore, hypothalamic lesions following 5,7-DHT increase lordosis, but fail to unmask in males the responsiveness to E + P priming proceptive behaviours by females. Further, the levels of lordosis responding displayed by lesioned males are lower than those of either lesioned or control females after E + P priming, as well as those of lesioned females after E priming alone, thus indicating that other inhibitory mechanisms continue to operate in the lesioned males.

Animals↗
PubMed1988

Alpha-1- and alpha-2-noradrenergic receptors modulate lordosis behavior in female guinea pigs.

Modulation of lordosis behavior by stimulation of noradrenergic receptor subtypes was examined in ovariectomized, estradiol benzoate (10 micrograms)-primed guinea pigs. In the first experiment, subcutaneous administration of the alpha-2-noradrenergic agonist, UK-14,304 (0.01, 0.5, or 1.0 mg/kg, Pfizer Central Research), produced a significant increase in lordosis behavior when these animals were compared with estrogen-primed control animals injected with saline. In a second experiment, estrogen-primed animals were injected with the alpha-1-noradrenergic agonist methoxamine (0.5 mg/kg, s.c.), UK-14,304 (0.5 mg/kg, s.c.), or both drugs given together. Methoxamine or UK-14,304 administered alone facilitated lordosis in fewer than 50% of animals (17 and 39%, respectively). However, when both drugs were given together, 76% of the animals became sexually receptive. A third experiment showed that lordosis behavior facilitated by UK-14,304 could be attenuated by the administration of the alpha-2-noradrenergic antagonist idazoxan (2.5 mg/kg, s.c.). Only 29% of sexually receptive animals (i.e. those animals primed with estradiol benzoate plus UK-14,304) continued to show lordosis after they received idazoxan. The results obtained from these and previously reported experiments suggest that both alpha-1- and alpha-2-noradrenergic receptors are involved in the regulation of lordosis behavior in the guinea pig.

Animals↗
PubMed1979

A sexually dimorphic rhythm in oestradiol-activated lordosis behaviour in the rat.

Ovariectomized rats exposed to constant plasma levels of oestradiol showed a daily rhythm in lordosis behaviour, with high levels of lordosis occurring during the dark portion of the daily light: darkness cycle and low levels during the light period. Similarly treated male rats failed to show a rhythm in lordosis behaviour. However, neonatal castration permitted the expression of the lordosis rhythm in male rats; conversely, an injection of 1.25 mg testosterone propionate on day 4 of life abolished the rhythm in female rats. Pinealectomy, adrenalectomy or depletion of brain 5-hydroxytryptamine levels did not affect the periodicity in lordosis behaviour but lesions in the suprachiasmatic nuclei of the hypothalamus disrupted the rhythm. It is suggested that the daily rhythm in lordosis behaviour participates in the control of the termination of heat in the female rat and that the perinatal hormone milieu may exert permanent effects on periodic functions.

Animals↗
PubMed2003

Effects of highly or relatively selective 5-HT1A receptor agonists on lordosis in female rats.

To investigate the role of serotonin (5-HT) receptor 1A or 7 in regulating lordosis behavior in female rats, ovariectomized rats were treated with 3 kinds of receptor agonists and lordosis behavior was observed. The injected agents were the selective 5-HT1A receptor agonist, buspirone (BUS), the highly selective 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin ((+/-)8-OH-DPAT), and the 5-HT1A and 5-HT7 receptor agonist, (R)-8-hydroxy-2-(di-n-propylamino)tetralin ((+)8-OH-DPAT). A behavioral test was performed after ovariectomy and subcutaneous implantation of a silicon tube containing estradiol. Female rats in which the lordosis quotient (LQ) was over 70 were intraperitoneally injected with several doses of these agents. As a result, in the BUS group, the dose of 3 mg/kg bw, but not 1 mg/kg was effective for suppressing lordosis. On the other hand, an inhibitory effect was observed from 0.25 mg/kg and 0.5 mg/kg in the (+)8-OH-DPAT and (+/-)8-OH-DPAT groups, respectively. In the time-course experiment, in all drug-treated groups, LQ decreased to lower than 20 after 15 min and low LQ continued for 1 hr at least. Measurement of locomotor activity using an infrared sensor system showed no relation between the decrease in lordosis by these agents and spontaneous locomotion. These results indicate that 5-HT1A is strongly involved in the lordosis-inhibiting circuit of the serotonin neurons.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

[A study of urinary immunoglobulin excretion after forced lordosis].

Changes in the urinary excretion of immunoglobulins (IgG and IgA) before and after forced lordosis were studied in 26 children with orthostatic proteinuria (group OA, where proteinuria disappeared within 120 min after lordosis was referred to as group OAA and where if disappeared after more than 120 min was group OAB) and 9 children with chronic glomerulonephritis in the clinically stable state (group GN). Urinary immunoglobulins were measured by ELISA (enzyme linked immunosorbent assay). In resting urine, the urinary excretion rates (total protein, IgG, and IgA) and the urinary protein ratio (IgG/protein, IgA/protein, and IgA/IgG) did not significantly differ between groups OA and GN. When forced lordosis was carried out, at maximum protein excretion, the urinary IgA/IgG ratio in groups OAA and OAB were significantly decreased (from 198 + 44% to 17.3 + 12.9% and from 147 + 88% to 18.7 + 16.9%, respectively). The ratio of IgA/IgG in groups OAA and OAB was significantly lower than that in group GN (88.9 + 53.9%, p less than 0.01). The urinary IgA/IgG ratio after lordosis in group OA was similar to the serum IgA/IgG ratio. These findings suggest that transient low or non-selective proteinuria after lordosis is a characteristic of orthostatic proteinuria. Analysis of the urine after forced lordosis, especially using the urinary IgA/IgG ratio at maximum protein excretion, may be an useful examination for differentiating OA from other glomerulonephritides.

Adolescent↗
PubMed1979

Deficit in the lordosis reflex of female rats caused by lesions in the ventromedial nucleus of the hypothalamus.

1. The effect of electrolytic lesions of the ventromedial nucleus of the hypothalamus (v.m.n.) on the lordosis reflex has been investigated on ovariectomized female rats. Lesions were made through chronically implanted platinum-iridium electrodes. 2. V.m.n. lesions did not disrupt lordosis immediately, but induced a gradual decline in the reflex. Lordosis performance reached it minimum no less than 12 hr after the lesion, and typically after 36--60 hr. 3. The magnitude of the lordosis deficit was related to the amount of v.m.n. damage. Destruction of other hypothalamic regions was without appreciable relation to the deficit. Within v.m.n., lesion size in the lateral, but not medial portion was significantly correlated with lordosis deficit. 4. Because of the slow time courses of v.m.n. lesions and stimulation (Pfaff & Sakuma, 1978) effects, it is postulated that the v.m.n. is not part of the direct reflex-arc for lordosis. Rather, neurones in v.m.n. are likely to exert a tonic hormone-dependent bias on brain stem reflex paths for this behaviour.

Animals↗
PubMed1983

Effect of guanine derivatives on lordosis behavior in estrogen primed rats.

The effect of systemic administration of guanosine, cGMP, dipalmitoyl (dp) cGMP, 5'GMP and 5'GDP on lordosis behavior was studied in ovariectomized, estradiol benzoate (EB) primed rats (4 micrograms/rat). EB per se induced only weak lordosis behavior. Free cGMP (2.0 mg/rat); dp cGMP (1.0, 2.0 and 4.0 mg/rat) and 5'GMP (2.0 and 4.0 mg/rat) induced significant lordosis behavior in ovariectomized, estrogen-primed rats. Dp cGMP and 5'GMP (2.0 mg/rat), also induced lordosis behavior in ovariectomized, adrenalectomized estrogen primed rats. Lordosis behavior elicited with 2.0 mg/rat dp cGMP was blocked with 8.0 mg/rat methyl-isobutylxanthine (MIX), a phosphodiesterase inhibitor, suggesting that dp cGMP stimulated lordosis through its conversion to 5'GMP. Results are interpreted in terms of the activation of adenylate cyclase-cAMP systems by guanine nucleotides.

1-Methyl-3-isobutylxanthine↗