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PubMed2000

Retroambiguus projections to the cutaneus trunci motoneurons may form a pathway in the central control of mating.

Our laboratory has proposed that the nucleus retroambiguus (NRA) generates the specific motor performance displayed by female cats during mating and that it uses direct pathways to the motoneurons of the lower limb muscles involved in this activity. In the hamster a similar NRA-projection system could generate the typical female mating posture, which is characterized by lordosis of the back as well as elevation of the tail. The present study attempted to determine whether this elevation of the tail is also part of the NRA-mating control system. The basic assumption was that elevation of the tail is a function of the cutaneous trunci muscle (CTM), which was verified by bilateral tetanic stimulation of the lateral thoracic nerves innervating the CTM. It resulted in upward movement of the tail to a position similar to the tail-up position during the lordosis posture. Retrograde tracing results showed that CTM motoneurons are located in the ventral and ventrolateral part of the C(7)-C(8) ventral horn, those innervating the tail region ventrolateral to those innervating the axillary region. Anterograde tracing studies showed that NRA fibers terminate bilaterally in both parts of the CTM motoneuronal cell groups. Electron microscopical studies revealed that labeled NRA terminals make monosynaptic contacts with retrogradely labeled dendrites of CTM motoneurons. Almost all of these terminal profiles had asymmetric synapses and contained spherical vesicles, which suggests an excitatory function. The observation that 15% of the labeled NRA terminals make more than one synaptic contact with a retrogradely labeled CTM motoneuronal dendrite within the same section indicates how powerful the NRA-CTM projection is. The results indicate that during mating the NRA not only could generate the lordosis posture but also the elevation of the tail.

Animals↗
PubMed2003

Central insulin administration maintains reproductive behavior in diabetic female rats.

Diabetic female rats have decreased ovulation, reproductive behavior and luteinizing hormone surges. Peripheral insulin treatment restores the phenotype to normal and also corrects many of the metabolic changes. To further evaluate the role of insulin in the specific maintenance of reproductive behavior, rather than administering it peripherally, we gave insulin intracerebroventricularly (ICV) at doses that did not correct the peripheral metabolic changes associated with diabetes such as hyperglycemia. During the experiment, we assessed the general activity and reproductive behavior of gonadectomized, estrogen- and progesterone-treated diabetic and control, nondiabetic female rats. Some of the animals received ICV saline, the rest received ICV insulin. General activity (ambulation, rearing and corner sniffing) was not affected by any of the treatments. Streptozotocin-induced diabetes resulted in a significantly decreased lordosis quotient, and ICV insulin was able to completely prevent this reduction. Furthermore, ICV insulin was able to cause a modest increase in the lordosis quotient among nondiabetic rats as well. Moreover, ICV insulin also increased the quality of lordosis among diabetic rats. Our results support a central role of insulin in the control of reproductive functions, beyond maintaining the homeostatic and metabolic balance.

Analysis of Variance↗
PubMed1981

Effect of neonatal intrahypothalamic testosterone implants on cyclicity and adult sexual behavior in the female hamster.

To localize the neural sites of hormone action for sexual differentiation in the hamster, pellets containing 3 microgram testosterone were implanted directly in the preoptic area-anterior hypothalamus (POA-AH) and the ventromedial hypothalamus-arcuate regions of the hypothalamus of 3-day-old female hamsters. The POA-AH implants strongly enhanced the potential for ectopic mounts, rear mounts, and intromission patterns after adult testosterone treatment. 50% of the females with neonatal POA-AH implants demonstrated vaginal acyclicity in adulthood, suggesting a significant disruption of normal gonadotropin release. Tests for female sexual behavior revealed that implants in both POA-AH and ventromedial arcuate had no significant effect on latency to lordosis or total lordosis duration with estrogen and progesterone priming, but did reduce the longest single bout of lordosis. In conjunction with other recent investigations, these findings suggest that in the hamster, as in other species, androgenization involves several independent processes in terms of both location and sensitivity to hormone exposure.

Animals↗
PubMed1983

Progesterone enhancement of lysergic acid diethylamide and levo-5-hydroxytryptophan stimulation of the copulatory response in the female rat.

Copulatory behavior in the ovariectomized rat, i.e. the lordosis response (LR) on being mounted by a male, can be induced by administration of either estrogen alone or estrogen followed by progesterone. LR has been shown to be inhibited by lysergic acid diethylamide (LSD) in certain doses (greater than or equal to 50 micrograms/kg) and by Levo-5-hydroxytryptophan (L-5-HTP) (greater than or equal to 2.5 mg/kg). This effect was recently found to be enhanced by increasing doses of progesterone. In contrast, small doses of LSD (5-30 micrograms/kg) have been shown to increase LR activated by estrogen alone. The effects of various hormone treatments on the stimulatory action of LSD were tested in the present study. When the lordosis behavior was activated by estradiol benzoate (EB) alone (25 or 7 X 2 micrograms/kg), LR increased 10 min after injection of LSD in a dose of 10 micrograms/kg. There were no detectable effects in animals treated with estrogen alone when the dose of LSD was lowered to 1 microgram/kg. LSD in the latter dose gave an increased response, however, when LR was activated by EB (5 micrograms/kg) in combination with progesterone (4.0 mg/rat). An analogous study was conducted with L-5-HTP, after pretreatment with pargyline and R04-4602. Small doses of L-5-HTP (0.25 and 0.05 mg/kg) stimulated the LR and the influence of progesterone was the same as for small doses of LSD. Possible mechanisms underlying the observed influence of progesterone on serotonergic mechanisms involved in the lordosis behavior are discussed.

5-Hydroxytryptophan↗
PubMed1986

Suppression of receptive and proceptive behavior in ovariectomized, estrogen-progesterone-primed rats by intraventricular beta-endorphin: studies of behavioral specificity.

Intraventricular (i.c.v.) administration of beta-endorphin (beta-END) has been shown to suppress lordosis behavior in ovariectomized (OVX) estrogen-progesterone (EP) primed rats, but the behavioral specificity of this effect is not known. Using OVX EP-primed rats, the present study assessed the effect of i.c.v. beta-END on proceptive behavior as well as on lordosis (receptive) behavior, and attempted to discern whether the sexual effects were secondary to generalized nonspecific behavioral effects. Doses of 0.5-4 micrograms beta-END (human) significantly suppressed lordosis behavior. Doses of 1 and 4 micrograms were used in experiments which measured proceptive behaviors (presentations and ear wiggling), and both doses abolished or nearly abolished the display of these behaviors. Administration of inactive peptide (a protein digest) had no effect on sexual behavior. Neither 1 nor 4 micrograms beta-END elicited measurable catalepsy. In a series of tests for responsiveness to general somatosensory stimuli, 1 microgram had no effect on responsiveness while 4 micrograms had minor effects, even though sexual activity was severely diminished after both doses. Blood pressure was unaltered by infusion of beta-END (1 microgram), although there was a significant reduction in heart rate. When open field behavior was tested in conjunction with sexual behavior, ambulation and rearing were significantly decreased after beta-END treatment as compared with saline treatment. However, simple linear correlation tests showed a lack of correlation between the changes in open field behavior and the changes in sexual behavior, indicating that the effects of beta-END on the two types of behavior may be unrelated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Ovarian steroid and growth factor regulation of female reproductive function involves modification of hypothalamic alpha 1-adrenoceptor signaling.

The ovarian steroids estradiol (E(2)) and progesterone (P) act on target neurons in the hypothalamus and preoptic area to coordinate the expression of female reproductive behaviors with the timing of the preovulatory luteinizing hormone (LH) surge. This chapter will summarize evidence that E(2) and P facilitation of the receptive component of female reproductive behavior, lordosis, involves changes in both the expression of and intracellular signal transduction pathways engaged by alpha(1)-adrenergic receptors in the hypothalamus and preoptic area. The alpha(1)-adrenoceptors are thought to mediate the facilitatory effects of the catecholamine neurotransmitter norepinephrine on both lordosis behavior and LH release. E(2) first induces the expression of the alpha(1B)-adrenergic receptor subtype in the hypothalamus and preoptic area. P then acts in an E(2)-dependent manner to promote linkage of hypothalamic alpha(1)-adrenoceptors to an intracellular signaling pathway involving nitric oxide and cyclic GMP. This chapter will also describe recent findings that implicate brain insulin-like growth factor-I (IGF-I) receptors as obligatory co-mediators of hormonal regulation of hypothalamic alpha(1)-adrenoceptors and female neuroendocrine function. Additional studies suggest that E(2) and IGF-I facilitate lordosis behavior by activating kinases traditionally associated with growth factor signal transduction (mitogen-activated protein kinases and phosphatidlyinositol-3-kinases). These molecular events are proposed to help coordinate the timing of ovulation with the expression of sexual receptivity, thereby maximizing reproductive success.

Animals↗
PubMed2003

Hormonal-neural integration in the female rat ventromedial hypothalamus: triple labeling for estrogen receptor-alpha, retrograde tract tracing from the periaqueductal gray, and mating-induced Fos expression.

The lordosis reflex, a stereotypic posture adopted by female rats during sexual behavior, requires the convergence of a hormonal signal, estrogen, with a descending neural pathway from the ventromedial hypothalamic nucleus (VMH). The VMH contains at least three lordosis-relevant neural populations: estrogen receptor-alpha immunoreactive (ERalpha-IR) neurons, VMH neurons that project to the periaqueductal gray (PAG), and neurons that are ERalpha-IR and project to the PAG. Expression of Fos, a marker for neuronal activation, is increased in the VMH after mating. However, it is unknown which, if any, of these lordosis-relevant populations is activated. The majority of ERalpha-IR and projection neurons were not colocalized. Of the Fos-positive neurons, 41% neither contained ERalpha nor projected to the PAG, and 35% contained ERalpha but did not project to the PAG. Only 25% of Fos-positive neurons projected to the PAG, including projection neurons that expressed ERalpha. Our results suggest that mating activates several distinct VMH neuron types. However, ERalpha-IR neurons are activated to a greater extent compared with the PAG-projecting neurons.

Animals↗
PubMed1982

1-(o-chlorophenyl)-1-(p-chlorophenyl)2,2,2-trichloroethane: a probe for studying estrogen and progestin receptor mediation of female sexual behavior and neuroendocrine responses.

A number of chlorinated insecticides have been shown to interact with estrogen receptors and to mimic estrogen action in peripheral reproductive tissues (e.g. vagina and uterus). The present study was designed to assess whether the dichlorodiphenyltrichloroethane (DDT) isomer o,p'-DDT has estrogenic or antiestrogenic activity in neural estrogen target tissues. Single sc injections of up to 500 mg/kg o,p'-DDT had no effect on female sexual behavior (lordosis). However, more prolonged treatments induced high levels of lordosis behavior, inhibited compensatory ovarian hypertrophy, and reduced body weight gain in ovariectomized adult female rats. Since o,p'-DDT was able to mimic the action of estrogen on these three neuroendocrine responses, further experiments were performed to determine whether the compound could be used as a tool to investigate the role of hypothalamic steroid receptors in estrogen stimulation of reproductive behavior. It was found that single injections of 500 mg/kg o,p'-DDT (which did not induce sexual receptivity) interacted with cytosol estrogen receptors in both the hypothalamus and pituitary. However, depletion of cytosol receptors by o,p'-DDT was very slow and incomplete; maximal depletion was only 51% and did not occur until 8 h postinjection. It was also observed that neither behaviorally effective nor ineffective injections of o,p'-DDT were able to induce progestin receptor synthesis in the hypothalamus or pituitary. Thus, it appears that the inability of the compound to promote lordosis behavior after a single injection probably results from inadequate receptor interaction in hypothalamic cell nuclei, but that failure to induce neural progestin receptor synthesis is not the critical factor. These data also suggest that the study of o,p'-DDT action in the brain may provide useful information regarding mechanisms of steroid mediation of neuroendocrine responses.

Animals↗
PubMed1986

Antagonism of female sexual behavior with intracerebral implants of antiprogestin RU 38486: correlation with binding to neural progestin receptors.

The steroidal antiprogestin 17 beta-hydroxyl-11 beta-(4-dimethylaminophenyl)-17 alpha-(1-propynl)estra-4,9-dien-3-one (RU 38486) was administered systemically or was implanted into the ventromedial hypothalamus and other brain regions (habenula, preoptic area, interpeduncular region, in order to determine whether the compound could antagonize progesterone (P) activation of estrous responsiveness and whether the compound would exert its behavioral effects at the presumed site of P action and/or at other neural sites implicated in the regulation of female sexual behavior. RU 38486 (5 mg) administered sc 1 h before 200 micrograms P inhibited P facilitation of lordosis behavior in estrogen-primed rats. Intracerebral application of RU 38486 to the ventromedial hypothalamus reduced lordosis responses in 14 of the 25 animals tested. Similar implants in the habenula also inhibited lordosis in 5 of the 14 animals tested. Antiprogestin implants in the interpeduncular region and preoptic area were virtually without effect (1 of 7 inhibited in each group). Interactions of RU 38486 with steroid binding sites in the hypothalamus-preoptic area (HPOA) were also assessed. RU 38486 appeared to be a competitive inhibitor of progestin ([3H] R5020) binding in HPOA cytosols. Scatchard analysis of [3H]RU 38486 binding showed that when unlabeled P was used as the competitor to assess nonspecific binding, the antiprogestin bound with high affinity [dissociation constant Kd = 8.4 nm] to brain cytosols. In addition, the number of [3H]RU 38486 binding sites in HPOA cytosol increased by approximately 50% in estrogen-primed female rats. Competition studies indicated that unlabeled RU 38486 was the most effective competitor for [3H]RU 38486 binding but that P and R5020 were nearly as effective. Corticosterone, hydrocortisone, deoxycorticosterone, and triamcinolone also competed for [3H]RU 38486 binding but were somewhat less effective than the progestins. Testosterone and estradiol did not displace [3H]RU 38486 except at very high molar excesses. Thus RU 38486 appears to bind with highest affinity to HPOA progestin receptors, but it also binds to glucocorticoid receptors. These data are consistent with the interpretation that inhibition of estrous responsiveness by RU 38486 is associated with the antagonist's interference with brain progestin binding.

Animals↗
PubMed1989

Dilute estradiol implants and progestin receptor induction in the ventromedial nucleus of the hypothalamus: correlation with receptive behavior in female rats.

The ventromedial nucleus of the hypothalamus (VMN) is thought to constitute an essential neural substrate for hormonal induction of female sexual behavior. In previous work, implants of dilute (0.4%) estradiol (E2) have been found to prime progesterone-facilitated female sexual behavior in rats only when they are within or very close to the VMN. In other studies, induction of cytosolic progestin receptors (PRc) in the hypothalamus has been correlated with systemic E2 priming of receptive behavior. We combined dilute E2 implants with a Palkovits punch microassay for PRc in the an effort to examine the relationship between estrous behavior and estrogen-induced PRc in the VMN of individual female rats. Ovariectomized rats were given bilateral guide cannulae aimed at the VMN and were primed for 3 days with 1) blank implants plus oil sc, 2) blank implants plus 0.5 micrograms E2 benzoate sc, 3) implants of 0.4% E2 in cholesterol, or 4) implants of 2.0% E2. On day 4 all rats received progesterone (P) sc and were tested for receptive behavior. The following week all subjects received the same estrogen-priming treatment but were killed on day 4 without P treatment. The VMN was punch dissected and assayed for PRc. High levels of lordosis were seen in the E2 benzoate-treated and 2.0% E2-implanted animals, while little behavior was seen in the oil-treated animals. Among 0.4% E2-implanted animals, higher levels of lordosis were observed in subjects with implant placements in the rostral than in the caudal VMN; however, lordosis quotients were not correlated with PRc induction measured in the entire VMN of individual animals. In general, our findings suggest that local estrogenic stimulation of target cells in the VMN is capable of both priming the estrous response and induction of P receptors. Whether these two effects are causally related awaits future study.

Animals↗
PubMed1975

Effects of testosterone propionate or dihydrotestosterone propionate on plasma FSH and LH levels in neonatal rats and on sexual differentiation of the brain.

The present study tests the hypothesis that the effects of perinatal androgen administration on the development of the brain are brought about indirectly by a suppression of plasma gonadotropin (GTH) titers. Both castrated male and intact female rats were treated neonatally with 5 alpha-dihydrotestosterone propionate (DHTP) or testosterone propionate (TP) throughout the first ten postnatal days of life and the corresponding effects on neonatal plasma FSH and LH levels and the subsequent ability of the adult to exhibit cyclic GTH release and female sex behavior (lordosis) were determined. In males castrated within 24 h of birth, subcutaneous injections of DHTP (60 or 180 mug per 100 g average body weight) or TP (60 mug/100 g) given on day 2, 4, 6, 8 and 10 reduced plasma levels of FSH and LH as determined by radioimmunoassay 48 h following the first and last injections. However, TP but not DHTP masculinized the development of the regulation of GTH release as mesured by luteinization of subcutaneous ovarian grafts, and also suppressed the ability of adult neonatally castrated male primed with estradiol benzoate and progesterone to display lordosis behavior. In intact females, the same neonatal DHTP and TP injection regime lowered FSH and LH plasma levels following the last injection (day 12), while DHTP lowered LH, but not FSH, following the first injection (day 4). All TP treated females had ovaries devoid of CL by 45 days of age and showed prolonged vaginal cornification. However, DHTP failed to masculinize the pattern of GTH release in females since DHTP-treated females, like oil-treated females, possessed CL(days 45 and 100) and exhibited vaginal cycles (days 80-100). Lordosis quotients of females treated neonatally with DHTP were as high as those of oil-treated females and significantly higher than those of TP-treated females. These results demonstrate that the ability of TP to induce maculine differentiation of the neural regulation of GTH release and female sex behavior does not depend on its ability to depress circulating LH and FSH levels in the neonatal male, or LH levels in the neonatal female rat.

Animals↗
PubMed1997

Abnormal estrous cyclicity and behavioral hyporesponsiveness to ovarian hormones in genetically obese Zucker female rats.

Obese Zucker female rats are infertile. The present study was designed to assess estrous cyclicity in adult, ovary-intact, lean and obese Zucker rats and to compare reproductive behaviors induced by exogenous steroid hormones in ovariectomized (ovx) lean and obese Zucker rats. The majority (90%) of obese rats had incomplete cycles in comparison with the normal, 4-day cycles displayed by lean Zucker rats. After ovariectomy, all rats were treated with estradiol benzoate (EB, 15-100 micrograms/kg) or EB plus progesterone (P, 2-20 mg/kg), and tested for sexual receptivity and proceptivity (PRO). At the highest EB dose, obese Zucker females displayed lordosis less frequently than lean rats (lordosis quotient, LQ, 8 +/- 6% vs. 32 +/- 13%, respectively). At the lowest doses of EB plus P, lean females were extremely receptive and proceptive (LQ = 93 +/- 4%, PRO = 6.2 +/- 2 bouts/min). Zucker obese females, in contrast, were only slightly receptive (LQ = 26 +/- 11%) and showed less PRO than lean rats (PRO = 2.4 +/- 0.6 bouts/min). Increasing the dose of either EB or P, administered in combination with the lowest dose of the other hormone, produced receptivity and PRO in obese Zucker females that were comparable with those observed in lean rats. Serum estradiol and P levels in ovx obese rats were either equivalent to or higher than those in the ovx lean rats when both were given the same doses of hormones. These data suggest that considerably higher doses and serum concentrations of EB and/or P are required to elicit robust lordosis and PRO in ovx obese Zucker than in lean rats. This behavioral hyporesponsiveness to sex steroid hormones may contribute to infertility in the obese Zucker female rat.

Animals↗
PubMed2002

Sex difference in septal neurons projecting axons to midbrain central gray in rats: a combined double retrograde tracing and ER-immunohistochemical study.

Sex difference in the number of neurons projecting axons from the lateral septum (LS) to the midbrain central gray (MCG) that are concerned with the lordosis-inhibiting system was investigated by injection of Fluoro-Gold (FG), a retrograde tracer, into the rostral MCG on the right side in male and female rats. Immunohistochemistry for ER-alpha and -beta was also performed with or without combination with FG immunostaining. All animals were gonadectomized. Lordosis was observed after treatment with E2 in some animals. In the results, lordosis was rare in males, compared with females. FG-immunoreactive (ir) cells were concentrated in the intermediate LS on the right side, and its number in the females was significantly higher than that in the males. There was no sex difference in the distribution and number of ERalpha-ir and ERbeta-ir cells in the LS. Furthermore, the number of ERs-ir cells was not influenced by E2 in either males or females. Double FG-ERbeta-ir cells were less than 20% of total FG-ir cells in the LS in both males and females. These data suggest that the LS-MCG connection is sexually dimorphic but that there is no sex difference in the expression of ERs in the LS.

Animals↗
PubMed2000

Epidermal growth factor activates reproductive behavior independent of ovarian steroids in female rodents.

Sex steroids exert profound influence on neural development and function through activation of intranuclear receptors. However, during sexual differentiation and at onset of puberty, intracerebral estrogen (E) availability is subsequent to these effects. The potent mitogen epidermal growth factor (EGF) activates estrogen receptor (ER)-dependent transcription in cultured cells in the absence of exogenous E. Since reproductive behavior in female rodents is the result of E-dependent transcriptional activity and protein synthesis, lordosis serves as a well established in vivo model for probing cellular and molecular mechanisms of steroid receptor-dependent behavior. Here we demonstrate that EGF can signal through the classical E receptor (ERalpha) to alter in vivo function in rodent central nervous system. EGF and EGF receptor ligands induced lordosis in a dose- and time-dependent manner in the absence of steroid treatment in ovariectomized rats and mice. Using antisense oligonucleotides, pharmacological and antibody blockade, and mutant mice, we also report that this behavioral responsiveness is mediated through ERalpha by specific stimulation of membrane-bound EGF receptors and EGF receptor-specific tyrosine kinase rather than by direct ligand activation of the ERalpha. Of biological significance, delayed onset of puberty and the absence of synchronization between reproductive behavior and ovulation was detected in intact mutant Wa-2 mice that express a naturally occurring point mutation in the EGF receptor. To our surprise, EGF-mediated behavior was independent of progesterone (P) and progesterone receptor (PR) since antiprogestins, PR antisense oligonucleotides, and targeted disruption of PR in ovariectomized transgenic mice failed to impede the display of lordosis after EGF. Finally, we also found that another growth factor, insulin-like growth factor-1, which provokes ER-dependent transcription in vitro, activates mating behavior in a similar E-independent manner. Thus, growth factor mediation of ER-targeted function may be a universal feature in the rodent central nervous system, raising critical questions about the role of growth factors in mediating ER-dependent processes in development and reproduction.

Aging↗
PubMed1984

Idiopathic scoliosis in three dimensions. A radiographic and morphometric analysis.

Eleven articulated scoliotic spines were examined radiographically and morphometrically. Measurement of the curve on anteroposterior radiographs of the specimens gave a mean Cobb angle of 70 degrees, though true anteroposterior radiographs of the deformity revealed a mean Cobb angle of 99 degrees (41% greater). Lateral radiographs gave the erroneous impression that there was a mean kyphosis of 41 degrees while true lateral projections revealed a mean apical lordosis of 14 degrees. Morphometric measurements confirmed the presence of a lordosis at bony level, the apical vertebral bodies being significantly taller anteriorly (P less than 0.02). There were significant correlations (P less than 0.01) between the true size of the lateral scoliosis, the amount of axial rotation and the size of the apical lordosis. This study illustrates the three-dimensional nature of the deformity in scoliosis and its property of changing in character and magnitude according to the plane of radiographic projection.

Anthropometry↗
PubMed2004

Estrogen-induced mu-opioid receptor internalization in the medial preoptic nucleus is mediated via neuropeptide Y-Y1 receptor activation in the arcuate nucleus of female rats.

The endogenous peptides beta-endorphin (beta-END) and neuropeptide Y (NPY) have been implicated in regulating sexual receptivity. Both beta-END and NPY systems are activated by estrogen and inhibit female sexual receptivity. The initial estrogen-induced sexual nonreceptivity is correlated with the activation and internalization of mu-opioid receptors (MORs), in the medial preoptic nucleus (MPN). Progesterone reverses the estrogen-induced activation/internalization of MOR and induces the sexual receptive behavior lordosis. To determine whether NPY and endogenous opioids interact, we tested the hypothesis that estrogen-induced MOR activation is mediated through NPY-Y1 receptor (Y1R) activation. Retrograde tract tracing demonstrated Y1Ron beta-END neurons that projected to the MPN. Sex steroid modulation of MOR in the MPN acts through NPY and the Y1R. Estradiol administration or intracerebroventricular injection of NPY activated/internalized Y1R in the arcuate nucleus and MOR in the MPN of ovariectomized (OVX) rats. Moreover, the selective Y1R agonist [Leu31, Pro34]-Neuropeptide Y (LPNY) internalized MOR in the MPN of OVX rats. The Y1R antagonist (Cys31, Nva34)-Neuropeptide Y (27-36)2 prevented estrogen-induced Y1R and MOR activation/internalization. NPY reversed the progesterone blockade of estradiol-induced Y1R and MOR internalization in the arcuate nucleus and MPN, respectively. Behaviorally, LPNY inhibited estrogen plus progesterone-induced lordosis, and the MOR-selective antagonist D-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr amide reversed LPNY-induced inhibition of lordosis. These results suggest that a sequential sex steroid activation of NPY and MOR circuits regulates sexual receptivity.

Animals↗
PubMed1993

The facilitatory effect of N-methyl-D-aspartate on sexual receptivity in female rats through GnRH release.

The purpose of this study was to examine whether N-methyl-D-aspartate affects the sexual receptivity of female rats. Monosodium L-glutamate was used as a neurotoxin to induce hypogonadal status. Matured normal and monosodium L-glutamate-treated rats were ovariectomized and implanted subcutaneously with estradiol capsules. One week later, lordosis responsiveness was observed before and 10 min after N-methyl-D-aspartate (40 mg/kg of BW, ip) administration. The results showed that N-methyl-D-aspartate caused a remarkable increase of lordosis quotient in control rats but not in monosodium L-glutamate-treated rats. Moreover, the possible action site of N-methyl-D-aspartate in the enhancement of receptivity was evaluated by the post-castrational LH rise, pituitary LH release in response to GnRH, and N-methyl-D-aspartate-evoked GnRH releasability. The results revealed that: (a) serum levels of LH in monosodium L-glutamate-treated rats were lower (p < 0.01) than those of control rats after ovariectomy; (b) there was no significant difference of pituitary LH release responsiveness to GnRH test between two groups; and (c) N-methyl-D-aspartate-evoked LH release in monosodium L-glutamate-treated rats was similar to that in the control rats. In conclusion, N-methyl-D-aspartate may facilitate the sexual receptivity through stimulating GnRH release. The failure of N-methyl-D-aspartate in enhancing receptivity in monosodium L-glutamate-treated rats is probably due to the cellular damage by monosodium L-glutamate on specific areas responsible for lordosis.

Animals↗
PubMed2003

Pedicle subtraction osteotomy for the treatment of fixed sagittal imbalance.

BACKGROUND: Fixed sagittal imbalance (a syndrome in which the patient is only able to stand with the weight-bearing line in front of the sacrum) has many etiologies. The most commonly reported technique for correction is the Smith-Petersen osteotomy. Few reports on pedicle subtraction procedures (resection of the posterior elements, pedicles, and vertebral body through a posterior approach) are available in the peer-reviewed literature. We are aware of no report involving a substantial number of patients with coexistent scoliosis who underwent pedicle/vertebral body subtraction for the treatment of fixed sagittal imbalance. METHODS: Twenty-seven consecutive patients in whom sagittal imbalance was treated with lumbar pedicle subtraction osteotomy at one institution were analyzed. Radiographic analysis included assessment of thoracic kyphosis, lumbar lordosis, lordosis through the pedicle subtraction osteotomy site, and the C7 sagittal plumb line. Outcomes analysis was performed with use of a before-and-after pain scale, items from the Oswestry questionnaire, and the Scoliosis Research Society (SRS) questionnaire after a minimum duration of follow-up of two years. Complications and radiographic findings were also analyzed for the entire group. RESULTS: Overall, the average increase in lordosis was 34.1 degrees and the average improvement in the sagittal plumb line was 13.5 cm. One patient had development of a lumbar pseudarthrosis through the area of pedicle subtraction osteotomy, and six patients had development of a thoracic pseudarthrosis. Two patients had development of increased kyphosis at L5/S1, caudad to the fusion, resulting in some loss of sagittal correction. There were significant improvements in the overall Oswestry score (p < 0.0001) and the pain-scale score (p = 0.0002). Most patients reported improvement in terms of pain and self-image as well as overall satisfaction with the procedure. CONCLUSIONS: Pedicle subtraction osteotomy is a useful procedure for patients with fixed sagittal imbalance. A worse clinical result is associated with increasing patient comorbidities, pseudarthrosis in the thoracic spine, and subsequent breakdown caudad to the fusion. LEVEL OF EVIDENCE: Therapeutic study, Level IV (case series [no, or historical, control group]). See Instructions to Authors for a complete description of levels of evidence.

Adult↗